Differential diagnosis and Differential diagnosis with functional gastric lesions

treatment of gastric dyspepsia lead biliary apparatus, acute and chronic exogenous dyspepsia and gastric
syndrome. dyspepsia. Modern methods of laboratory and instrumental examinations
  and treatment of chronic gastritis. Early diagnosis of gastric
cancer. Algorithms for examination of patients with suspected peptic
ulcer. Methods for diagnosing the presence of Helicobacter
pylori. Modern aspects of peptic ulcer treatment.

Definition of dyspepsia

The concept of dyspepsia (from Greek. "dys" – bad and "pepsis" - digestion) includes many subjective
symptoms that accompany a digestive disorder. Russian gastroenterologists traditionally consider dyspepsia
in a broad sense, i.e. as manifestations of diseases of the esophagus, stomach and intestines. These include:
abdominal pain, epigastric discomfort (heaviness, fullness, early satiety), excessive gas formation in the
intestines, heartburn, belching, dysphagia, nausea, vomiting, diarrhea, constipation, loss of
appetite. Dyspepsia is divided into functional and organic. Functional dyspepsia (with the presence of
characteristic complaints) with a thorough examination of patients is not accompanied by organic changes in
the organs of the gastrointestinal tract (GIT). Organic dyspepsia is associated with a serious organic disease
of the digestive tract. Manifestations of dyspepsia can be associated with food intake, or not depend on
it. Currently, foreign researchers define dyspepsia as chronic or recurrent pain or unpleasant sensations in
the upper abdomen. Unpleasant sensations mean subjective discomfort, but not pain, and may include: a
wide variety of symptoms, such as rapid satiety, bloating, a feeling of fullness in the epigastrium and
nausea. Apart from dyspepsia, foreign authors distinguish heartburn and acid belching, which are
manifestations of gastroesophageal reflux disease. Symptoms associated with intestinal pathology (diarrhea,
constipation, flatulence), according to foreign authors, do not fall under the term "dyspepsia". From our
point of view, it is advisable to divide dyspepsia into esophageal, gastric and intestinal. This facilitates the
differential diagnosis of diseases. Next, we will separately consider the manifestations of esophageal and
gastric dyspepsia and the clinical approach to patients with these manifestations.

Clinical assessment of patients with esophageal dyspepsia

Esophageal dyspepsia is characterized by dysphagia, heartburn, and belching. These symptoms can be

combined with individual diseases of the esophagus, but they can also occur independently of each other.

Dysphagia - this is the feeling of an obstacle to the normal passage of ingested food. Dysphagia is
considered as difficulty at the beginning of swallowing (oropharyngeal dysphagia), or as a feeling of
obstruction to the passage of food or liquid from the mouth to the stomach (esophageal dysphagia).

Dysphagia should be distinguished from other symptoms associated with swallowing. Aphagia means a

complete blockage of the esophagus, which is usually caused by a food lump stuck in the esophagus and
requires urgent medical intervention. Difficulty in trying to start swallowing occurs when the forced phase
of swallowing is disrupted. However, once started, the act of swallowing is completed
normally. Odynophagia means painful swallowing. Often, odynophagia and dysphagia develop
simultaneously. Odynophagia often indicates dysphagia in achalasia, diffuse esophageal spasm, and
esophagitis. Globus hystericus - this is the seeming sensation of a lump stuck in the throat. However, in the
actual implementation of the act of swallowing, there are no difficulties. Phagophobia means fear of
swallowing, and in cases of hysteria, rabies, tetanus and paralysis of the pharynx, refusal to swallow may
occur due to fear of aspiration. Painful inflammatory disorders that cause odynophagia can also lead to
refusal to swallow. Some patients may feel the process of food passing down the esophagus. However, this
sensitivity of the esophagus is not associated with food getting stuck in the esophagus or with its
blockage. Dysphagia should not be confused with the feeling of fullness in the epigastric region that occurs
after eating or after swallowing air.

Heartburn – this is a feeling of heat or burning, localized behind the sternum or in the upper part of the
epigastric region, with radiation to the neck, and sometimes in the forearm. Intermittent heartburn is also
common in healthy people, but frequent and severe heartburn is usually a manifestation of esophageal
dysfunction. Heartburn can be the result of impaired motor activity or stretching of the esophagus, throwing
acid or bile into the esophagus, or direct irritation of the esophageal mucosa (esophagitis). Heartburn is most
often associated with gastroesophageal reflux. In this case, heartburn develops after a heavy meal, when
bending or bending the body, or when the patient is lying on his back. It can be accompanied by the
spontaneous appearance of a liquid in the mouth, which can be salty ("sour belching"), sour (stomach
contents) or bitter, having a green or yellow color (bile). Heartburn can occur after consuming certain foods
(such as citrus juices) or medications (such as alcohol and acetylsalicylic acid). Usually, heartburn can be
alleviated immediately (at least temporarily) by taking antacids.

Heartburn can also occur in the absence of visible pathological conditions or disorders of motor function. In
this case, it is often accompanied by aerophagia, which may reflect the patient's attempt to relieve the feeling
of discomfort, and it is often attributed to psychological factors for lack of another explanation.

Burp – this is an involuntary sudden release of gases through the mouth from the stomach or esophagus,
sometimes with an admixture of a small amount of stomach contents, not accompanied by nausea and
vomiting. Belching can accompany heartburn.

Often in patients who complain of chronic, repeated burping, each act of regurgitation is preceded by
swallowing air, a large volume of which passes only part of the way down the esophagus, and then
regurgitates. Thus, an excessively intense belch occurs as a result of aerophagies (ingestion of air), and not
because of increased gas formation in the stomach or in the intestines. There is also a slight degree of
aerophagia in healthy people, but some people swallow excessive amounts of air due to a chronic state of
anxiety, rapid absorption of food, consumption of carbonated drinks, chewing gum, leakage of secretions
into the nasopharynx, or because of poorly fitted dentures. Because the belching that follows aerophagy can
give the patient a temporary sense of relief, a vicious cycle of swallowing air can develop, followed by
belching.

Diagnostic algorithm for dysphagia

The conclusion about the location of dysphagia should be made based on the patient's complaints; the lesion
will be located either in the place indicated by the patient's feelings, or below the specified location.

It is equally important to find out after taking what food (solid, liquid, or both) dysphagia occurs, whether it
is constant or intermittent. Determining the duration of symptoms is also important. Although they can often
occur together, it is important to rule out lonophagy (painful swallowing). Finally, differential diagnosis
based on the identification and analysis of symptoms should exclude the presence of Globus hystericus (a
lump in the throat), chest compression, difficulty breathing, and phagophobia (fear of swallowing).

When collecting complaints for dysphagia, it is necessary to find out:

• localization;

• nature of food and / or liquid;

• persistent or intermittent symptoms;

• duration of occurrence of symptoms.

The main question: is the dysphagia oropharyngeal or esophageal? This conclusion can be made with
confidence based on a very thorough examination, which provides an accurate assessment of the type of
dysphagia (oropharyngeal dysphagia compared to esophageal dysphagia occurs in 80-85% of cases).

Oropharyngeal dysphagia It can also be called "high" dysphagia if it is related to the oral cavity or
pharynx.

Patients have difficulty at the beginning of swallowing and they usually point to the cervical region as the
location of this difficulty.

Typical concomitant symptoms:

• difficulty at the beginning of swallowing;

• nasal regurgitation;

• cough;

• nasal speech;

• weakened cough reflex;

• choking attack;

• dysarthria or diplopia (may accompany neurological disorders that cause oropharyngeal dysphagia);

• bad breath may occur in patients with large Cenker diverticula containing residual food masses, as well as
with progressive achalasia or long-term obstruction of the lumen, leading to accumulation of decomposing
food.

An accurate diagnosis can be established after the neurological disorders accompanying oropharyngeal
dysphagia are clarified, these can be:

• hemiparesis caused by a stroke;

• ptosis of the eyelid;

• signs of myasthenia gravis in pregnant women (weakness by the end of the day);

• Parkinson's disease;
• other neurological diseases, including cervical dystonia, cervical hyperostosis, Arnold-Chiari
malformation (displacement of the brain in the caudal direction and pinching it in the large occipital
foramen);

• identification of a specific decrease in the number of brain nerves involved in the regulation of swallowing
can also help to accurately determine the cause of oropharyngeal disorders when making a diagnosis.

Esophageal dysphagia It can be called "lower" dysphagia, since it is mainly localized in the distal
esophagus, although it should be noted that some patients with esophageal dysphagia, such as achalasia, may
complain of difficulty swallowing in the cervical esophagus, which mimics oropharyngeal dysphagia. If
more than 2 seconds pass from the beginning of pharynx to signs of dysphagia, then this usually indicates
esophageal dysfunction.

The type of food consumed that causes dysphagia provides useful information. Difficulties that arise when
eating only solid food indicate the presence of mechanical dysphagia, in which the lumen is not narrowed so
much. A stuck food lump can be pushed through the narrowed area by drinking some liquid. With a
pronounced decrease in the lumen, dysphagia develops when eating both solid and liquid food. In contrast,
respiratory dysphagia caused by achalasia and diffuse esophageal spasm is equally affected by the use of
both solid and liquid food from the very beginning of the disease. Patients with scleroderma are susceptible
to developing dysphagia when eating solid food that is not related to the body position, while when eating
liquid food, dysphagia is observed in them in the supine position, but is absent when the body is upright. In
case of development of peptic strictures in such patients, dysphagia becomes more persistent.

Short-term transient dysphagia can be caused by any inflammatory processes. Progressive dysphagia over a
period of several weeks to several months suggests the presence of esophageal cancer. Episodic dysphagia
with solid food intake, which occurs for several years, indicates a benign disease and is characteristic of the
lower esophageal ring.

Establishing the location of dysphagia is of diagnostic value when it is described as tightness in the chest
area, where the location of dysphagia usually correlates with the location of esophageal
obstruction. However, the localization of dysphagia felt by the patient in the neck area has no diagnostic
value, since lesions of the pharynx, cervical esophagus, and even lower - lying areas of the esophagus can
cause dysphagia felt in the neck.

Concomitant symptoms have important diagnostic significance. Nasal regurgitation and tracheobronchial

aspiration during swallowing are signs of paralysis of the pharyngeal muscles or the presence of a
tracheoesophageal fistula. Non-swallowing tracheobronchial aspiration may be secondary in the presence of
achalasia, Cenker's diverticulum, or gastro-esophageal reflux. A pronounced decrease in body weight, not
proportional to the severity of dysphagia, is very characteristic of esophageal cancer. If dysphagia is
preceded by hoarseness, the primary lesion is usually localized in the larynx. Hoarseness that occurs after
the development of dysphagia, it may indicate involvement of the laryngeal recurrent nerve through the
spread of esophageal cancer beyond the walls of the esophagus. Sometimes hoarseness can be caused by
laryngitis, secondary to gastro-esophageal reflux. The combination of symptoms of laryngeal damage with
dysphagia is also observed in various neuromuscular disorders. Hiccups suggest a lesion of the distal
esophagus. Unilateral wheezing, combined with dysphagia, indicates a mediastinal process affecting the
esophagus and large bronchus. Chest pain the disease associated with dysphagia develops with diffuse
esophageal spasm and associated motor disorders. Chest pain, similar to the pain experienced with diffuse
esophageal spasms, can also occur in acute aphagia caused by too large a food lump. The presence in the
anamnesis of long-term heartburn and reflux preceding dysphagia indicates a peptic stricture. Similarly, a
history of prolonged nasogastric intubation, ingestion of caustic substances, previous radiation therapy, or
concomitant mucocutaneous diseases may indicate the cause of esophageal stricture. If the patient has
odynophagia, it should be assumed that he has candida or herpetic esophagitis, especially in weakened
cancer patients or in patients receiving immunosuppressive therapy.

Physical examination is important for motor dysphagia caused by skeletal muscle damage, neurological
diseases and diseases of the oropharynx. Carefully check for signs of bulbar or pseudobulbar paralysis, such
as dysarthria, dysphonia, ptosis, tongue atrophy, and overactive jaw muscle contractions, in addition to signs
of generalized neuromuscular disease. It is necessary to examine the neck area to make sure that there is no
enlargement of the thyroid gland or spinal disorders. Thorough examination the oral and pharyngeal cavity
should identify lesions that may prevent further passage of food from the mouth or esophagus due to pain or
obstruction. Changes in the skin or limbs may suggest a diagnosis of scleroderma and other collagen
diseases, or mucocutaneous diseases such as pemphigus or congenital epidermolysis bullosa, which can
cause damage to the esophagus. In addition, some patients with scleroderma and secondary peptic strictures
may have CREST syndrome (calcification, Raynaud's disease, esophageal motility disorders, sclerodactyly,
telangiectasia). There may be signs of metastatic damage to the lymph nodes and liver, as well as pulmonary
complications due to acute aspiration pneumonia or chronic aspiration of stomach contents.

Causes of esophageal dysphagia

Mucosal damage:

• gastroesophageal reflux disease (peptic stricture);

• esophageal rings and tissues (sideropenic dysphagia or Plummer-Vinson syndrome);

• esophageal tumors;

• caustic lesions of the esophagus (alkali ingestion, medicinal esophagitis, sclerotherapy of varicose veins);

• radiation damage;

• infectious esophagitis (candidiasis, herpes, cytomegalovirus).

Mediastinal diseases:

• tumors (including lung cancer, lymphoma);

• infections (including tuberculosis, histoplasmosis);

• cardiovascular diseases (left atrial dilatation, aortic aneurysm).

Diseases affecting the smooth muscles of the esophagus and its innervation:

• achalasia of the cardia;

• scleroderma;

• other motor disorders;

• condition after surgical operations (after fundoplication, antireflux operations, implantation of mechanical
devices).

The combination of progressive dysphagia when taking solid food and heartburn indicates the presence of
peptic stricture of the esophagus, and the combination of progressive dysphagia when taking liquid and solid
food with heartburn characterizes progressive systemic sclerosis (scleroderma). Foreign bodies in the
esophageal lumen usually cause acute dysphagia.

Symptoms of anxiety in esophageal and gastric dyspepsia

In addition to being over 50 years old, unexplained weight loss, anorexia, rapid satiety, vomiting,
progressive dysphagia, pain when swallowing, bleeding, anemia, jaundice, bulky formations in the
abdominal cavity, enlarged lymph nodes, cancer of the upper extremities are traditionally considered to be
alarming symptoms that indicate a possible serious disease, primarily a malignant neoplasm. GIT
departments in the next of kin, as well as data on past peptic ulcer disease, gastric surgery, or stomach
malignancies. In young patients in the absence of anxiety disorders malignancies of the upper
gastrointestinal tract are rare, but the predictive value of detecting alarming symptoms remains extremely
low. If the symptoms of dyspepsia have been observed for a long time, a malignant neoplasm is unlikely, but
what time period is meant when it comes to the prescription of symptoms, the literature does not
specify. Antisecretory therapy can mask a malignant tumor during esophagogastroduodenoscopy (EGDS),
but it does not affect the outcome of the disease. Although alarming symptoms do not always indicate a
serious illness, patients younger than 50 years of age with malignant neoplasms of the upper gastrointestinal
tract rarely do not have such symptoms. Alarming symptoms, and in patients over 50 years of age-any new
symptoms of dyspepsia, are indications for urgent EGDS to exclude a malignant tumor.

Instrumental diagnosis of esophageal dysphagia

The main task in the case of esophageal dysphagia is to exclude the malignant process.

Signs of malignancy of the process:

• the duration of the disease is short (less than 4 months);

• the disease is progressing;

• dysphagia is more pronounced when taking solid rather than liquid food.;

• there is weight loss.

The presence of the following signs indicates achalasia:

• dysphagia occurs after both solid and liquid food intake;

• the problem has existed for many years;

• no weight loss.

There are some disagreements regarding the choice of diagnostic tests, which relate to the choice of the
primary examination method – either endoscopy or barium ingestion.

Barium-contrast esophagogram
Barium esophagogram is performed in the supine position on the right side and allows you to identify
irregularities in the lumen of the esophagus and identify areas of obstruction, places of tissue damage and
rings. Barium testing of the oropharynx and esophagus during ingestion is the most appropriate initial test; it
may be useful for detecting achalasia and diffuse esophageal spasm, although this pathology can be more
accurately diagnosed by manometry. Such a study can be carried out using a barium tablet, which allows
you to identify even minor strictures. Examination of the esophagus after ingesting a barium tablet may also
be useful in patients with dysphagia in cases where the endoscopy results were negative.

Esophagogastroduodenoscopy It is performed using a fibrooptic endoscope passed through the mouth into
the stomach with detailed visualization of the upper gastrointestinal tract. The process of introducing an
endoscope into the stomach cavity is very important to exclude pseudoachalasia associated with a tumor of
the esophageal-gastric junction.

Esophageal manometry

This diagnostic method is less accessible than contrast/barium X-ray and endoscopy, but may be useful in
some cases. The method is based on measuring the pressure in the lumen of the esophagus using solid or
hydraulic measuring equipment.

Manometry is indicated for use in cases where it is assumed that the cause of esophageal dysphagia cannot
be detected either by X-ray examination or by endoscopy, and adequate anti-reflux therapy has been
performed (with the treatment of esophagitis, which is detected during endoscopy).

The three main causes of dysphagia that can be detected by manometry are: achalasia of the cardia,
scleroderma (ineffective peristalsis of the esophagus) and esophageal spasm.

Esophageal radionuclide scintigraphy

The patient swallows a liquid containing a radioactive label (for example, water mixed with Tc).99 and
colloidal sulfur) and then the radioactivity of the esophagus is measured. In patients with esophageal
contractility disorders, a slow release of the radioactive label from the esophagus is typical. This technique
was originally used for research purposes, but is now beginning to be used for clinical purposes in some
specialized institutes.

Diagnosis and treatment of diseases manifested by esophageal dyspepsia

In clinical practice, esophageal dyspepsia is most often found in gastroesophageal reflux disease, achalasia
of the cardia and esophageal cancer.

Gastroesophageal reflux disease and Barrett's esophagus

Gastroesophageal reflux disease (GERD) is a disease that manifests itself as a complex of characteristic
symptoms with the presence of inflammatory changes in the distal part of the esophagus, resulting from
repeated throwing of gastric and/or duodenal contents into the esophagus, or the presence of
gastro-esophageal reflux without concomitant inflammation of the esophagus.

Erosive gastroesophageal reflux disease is a type of reflux esophagitis (RE) that is accompanied by the
appearance of erosions on the surface of the esophageal mucosa.

Non-erosive gastroesophageal reflux disease (GERD) is characterized by the presence of reflux with or
without endoscopic manifestations of catarrhal RE. In non-erosive reflux disease, the diagnosis is
established on the basis of a typical clinical picture, taking into account data obtained with additional
research methods (pH-metric, X-ray, manometric). In the general population of patients with GERD,
individuals with NERD account for more than 60%. The severity of clinical symptoms and decreased quality
of life in patients with GERD are comparable to those in patients with erosive GERD.

Epidemiology

The prevalence of GERD among the adult population of Russia is up to 40-60%. In Western Europe and the
USA – up to 40%. The incidence of severe esophagitis in the general population is 5 cases per 100,000
population per year. The prevalence of Barrett's esophagus among individuals with esophagitis is close to
8%, with variations ranging from 5 to 30%. The presence of Barrett's esophagus increases the risk of
subsequent development of esophageal adenocarcinoma tenfold.

The formation of esophageal strictures was noted in 7-23% of patients with erosive-ulcerative esophagitis,
the occurrence of bleeding – in 2% of patients. Erosions and ulcers of the esophagus were the cause of
gastrointestinal bleeding in 21% of cases among people over 80 years of age, and in 25% of cases among
patients in intensive care units who underwent surgery.

Pathogenesis

The main pathogenetic factors for the development of clinical symptoms and morphological manifestations
of GERD are hydrochloric acid of the stomach and insufficiency of the lower esophageal sphincter. GERD
develops as a result of:

1) decrease in the function of the anti-reflux barrier, which can occur in three ways:: a) due to a primary
decrease in pressure in the lower esophageal sphincter; b) as a result of an increase in the number of
episodes of its spontaneous relaxation; c) due to its complete or partial destructurization, for example, with a
hernia of the esophageal opening of the diaphragm; d) other causes of insufficiency of the lower esophageal
sphincter: scleroderma, pregnancy, smoking, the use of drugs that reduce smooth muscle tone (nitrates,
calcium channel blockers, beta-adrenergic agents, eufillin), surgery on the sphincter;

2) reduced esophageal clearance: a) chemical – due to a decrease in the neutralizing effect of saliva and
bicarbonates of esophageal mucus; b) volumetric – due to inhibition of secondary peristalsis and a decrease
in the tone of the thoracic esophagus wall;

3) the damaging properties of refluktate (hydrochloric acid, pepsin, bile acids); 4) the inability of the
esophageal mucosa to resist the damaging effect of the thrown contents;

5) disorders of gastric emptying;

6) increased intra-abdominal pressure.

Clinical picture

The main symptoms of GERD are heartburn, belching, regurgitation, painful and difficult passage of
food. The quality of life of patients with GERD, who have clinical symptoms of the disease observed at
night, is particularly significantly reduced.

Heartburn is the most common symptom, occurs in 83 % of patients and occurs due to prolonged contact of
acidic (pH<4) gastric contents with the esophageal mucosa. Typical for this symptom is considered to
increase with errors in diet, alcohol intake, carbonated drinks, physical exertion, inclinations and in a
horizontal position. Belching, as one of the leading symptoms of GERD, is quite common and is found in
52% of patients. Belching, as a rule, increases after eating, taking carbonated drinks.
Regurgitation of food, which is observed in some GERD patients, increases with physical exertion and in a
position that promotes regurgitation. Dysphagia and lonophagia occur in 19% of patients with GERD. A
characteristic feature of these symptoms is their intermittent nature. Their occurrence is based on
hypermotor dyskinesia of the esophagus, which violates its peristaltic function, and the cause of
odynophagia can also be erosive and ulcerative lesions of the mucous membrane. The appearance of more
persistent dysphagia and a simultaneous decrease in heartburn may indicate the formation of esophageal
stricture.

One of the most characteristic symptoms of GERD is pain in the epigastric region, which appears in the
projection of the xiphoid process shortly after eating and increases when bending down.

Other symptoms of GERD include a lump in the throat when swallowing, pain in the lower jaw, and burning
of the tongue.

Extraesophageal manifestations of GERD

Among the extraesophageal manifestations of GERD, chest pain, similar to angina, and bronchopulmonary
symptoms are most common. Extraesophageal manifestations are very characteristic for non-erosive forms
of GERD.

Chest pains, including those similar to angina, occur in patients with GERD due to hypermotor dyskinesia of
the esophagus (secondary esophagospasm), which may be caused by a defect in the system of the inhibitory
transmitter – nitric oxide. The trigger point for the occurrence of esophagospasm and, accordingly, pain,
however, is always pathological (i.e. prolonged) gastro-esophageal reflux. In some cases, there is an
increased sensitivity of the receptors of the esophageal mucosa, the so-called "irritated"
esophagus. Abnormal reflux can also lead to cardiac arrhythmias.

Bronchopulmonary and laryngological manifestations of GERD include chronic cough, pneumonia,

bronchial asthma, obstructive pulmonary diseases, dysphonia, and laryngitis. Numerous foreign and
domestic studies have shown an increase in the risk of bronchial asthma, as well as the severity of its course
in patients with GERD. Gastroesophageal reflux is detected in 30-90% of patients with bronchial asthma,
predisposing to its more severe course. The causes of bronchial obstruction in GERD are: 1) vago-vagal
reflex, 2) microaspiration. Bronchopulmonary manifestations may be the only clinical sign of
gastroesophageal reflux and cause insufficient effectiveness of treatment of bronchial asthma. On the
contrary, the inclusion of drugs prescribed for GERD in complex therapy in such cases increases the
effectiveness of treatment of bronchial asthma.

Differential diagnosis

Clinical symptoms of GERD occur when tilted, in a horizontal position, combined with heartburn, belching,
stop when taking antacids, a sip of water.

The association of extraesophageal symptoms of GERD with episodes of pathological reflux can be most
accurately verified by 24-hour intraesophageal pH-metry. This method allows you to establish the presence
of a correlation between the appearance of pain and reflux episodes (symptom index > 50%). If pain
increases during exercise, combined pH and ECG monitoring can be performed (to exclude CHD). An
affordable method of differential diagnosis that has recently appeared can be considered the rabeprazole test,
the essence of which is the disappearance of the corresponding symptoms (heartburn, chest pain or
bronchopulmonary manifestations) within a day after taking 20 mg of rabeprazole. This method is based on
the ability of rabeprazole, unlike other PPIs, to stop the symptoms of GERD within the first 24 hours after
the start of use.
Complications

Complications of GERD include esophageal strictures, bleeding from esophageal ulcers, and Barrett's
esophagus. Strictures require further expensive surgical and endoscopic (and often repeated) procedures
(augmentation, surgical treatment, etc.). Bleeding caused by erosive and ulcerative lesions of the esophagus
can complicate the course of cirrhosis of the liver, and is also observed in patients who have undergone
surgery, and elderly patients. Among people over 80 years of age with gastrointestinal bleeding, erosions and
ulcers of the esophagus cause them in 20% of cases, and among patients in intensive care units who have
undergone surgery-in 25%.

Barrett's esophagus – this is a disease characterized by the replacement of the squamous epithelium of the
esophagus, normally lining its distal part, with a metaplastic cylindrical one. The name of the disease is
ironic and is given by the name of an English surgeon who claimed in his work that the esophagus cannot be
lined with cylindrical epithelium. Barrett's esophagus is pathogenetically closely associated with
gastro-esophageal reflux, as well as with esophageal adenocarcinoma and esophago-gastric junction. In
Barrett's esophagus, esophageal cancer is 40 times more common than in the rest of the
population. Exposure of hydrochloric acid in the esophagus, with On the one hand, it increases the activity
of protein kinases that initiate the mitogenic activity of cells and, accordingly, their proliferation, and, on the
other hand, inhibits apoptosis in the affected areas of the esophagus. Esophageal adenocarcinoma has a low
5-year survival rate, not exceeding 11%. Survival of patients depends on the stage of the disease, and one of
the unfavorable characteristics of esophageal adenocarcinoma should be considered early germination of the
walls of the organ and metastasis, which can occur long before the first clinical symptoms
appear. Approximately 95% of cases of esophageal adenocarcinoma are diagnosed in patients with Barrett's
esophagus. Therefore, the main role in the prevention and early diagnosis of esophageal cancer is played by
the diagnosis and effective treatment of Barrett's esophagus. After the use of proton pump inhibitors (PPIs)
in patients with Barrett's esophagus, a decrease in the level of proliferation markers is noted, which is absent
in those patients with persistent pathological acid reflux (pH<4). Proliferation activity also increases in those
patients who use H antagonists.2- histamine receptors (drugs that have much lower antisecretory activity
compared to PPIs). In turn, long-term use of PPIs leads to partial regression of a limited area of intestinal
metaplasia.

Among the risk factors for developing complications of GERD, the most important are the frequency and
duration of symptoms, in particular, heartburn, the severity of erosive esophagitis, the presence of a hiatal
hernia, and obesity with a body mass index of more than 30.

Rapidly progressing dysphagia and weight loss may indicate the development of esophageal
adenocarcinoma, but these symptoms occur only in the late stages of the disease, so clinical diagnosis of
esophageal cancer is usually delayed. Therefore, prevention and early diagnosis of esophageal cancer require
timely detection and adequate treatment of Barrett's esophagus.

Instrumental diagnostics

Endoscopic examination and classification of reflux esophagitis (RE)

Endoscopic examination may show signs of RE of varying severity: hyperemia and looseness of the
esophageal mucosa (catarrhal esophagitis, which belongs to the non-erosive form of GERD), erosion and
ulcers (erosive esophagitis of varying severity-from the 1st to the 4th stage-depending on the area of the
lesion), the presence of exudate, fibrin or signs of bleeding. In addition, prolapse of the gastric mucosa into
the esophagus may occur, especially with vomiting movements, true shortening of the esophagus with the
location of the esophageal-gastric junction significantly higher than the diaphragm, throwing gastric or
duodenal contents into the esophagus. It is rather difficult to assess the closing function of the cardia during
esophagoscopy, since the cardia can be slightly opened reflexively in response to the introduction of an
endoscope and air insufflation.

According to the Los Angeles classification, 4 degrees of RE are distinguished endoscopically:

Grade A – one (or more) mucosal lesion (erosion or ulceration) with a length of less than 5 mm, limited to
the limits of the mucosal fold;

Grade B – one (or more) mucosal lesion with a length of more than 5 mm, limited to the limits of the
mucosal fold;

Grade C - the mucosal lesion extends to 2 or more folds of the mucosa, but occupies less than 75% of the
circumference of the esophagus;

Grade D - mucosal damage extends to 75% or more of the circumference of the esophagus.

When making a diagnosis of GERD, the severity of reflux esophagitis (RE) is determined by the
Savary-Miller classification, which provides for the allocation of 4 (sometimes 5) degrees of severity of the
disease:

● RE of the first degree of severity - endoscopically isolated erosions that occupy less than 10% of the
surface of the mucosa of the distal esophagus;

● RE of the second degree of severity - erosions become draining and already capture 50% of the
surface of the mucous membrane of the distal esophagus;

● RE of the third degree of severity is characterized by the presence of circularly located drain erosions
that occupy almost the entire surface of the mucosa of the distal esophagus;

● RE of the IV degree of severity – the formation of peptic ulcers and strictures of the esophagus, as
well as the development of cylindrical metaplasia of the esophageal mucosa (Barrett's esophagus).

Some authors consider the last complication as V degree of severity of RE.

In many cases, the clinical symptoms of the disease are not accompanied by endoscopic and morphological
changes characteristic of erosive esophagitis (non-erosive form of the disease, NERD).

In case of torpid course of the disease (absence of clinical and endoscopic remission within 8 weeks of
standard adequate therapy), as well as the presence of complications of the disease (strictures, Barrett's
esophagus), it is necessary to conduct an examination in a specialized hospital or gastroenterological clinic,
including in outpatient departments of these institutions. If necessary, patients should undergo: histological
examination of esophageal mucosal biopsies to exclude Barrett's esophagus and adenocarcinoma,
esophageal manometry, pH-metric and X-ray studies.

Histological examination

More often, epithelial atrophy and thinning of the epithelial layer are detected, but occasionally, along with
atrophy, areas of epithelial layer hypertrophy can be detected. The stratification of the epithelium is
sometimes disturbed, while epithelial cells (epithelial cells) are in a state of dystrophy of varying degrees. In
some cases, dystrophy ends with necrosis of keratinocytes, especially pronounced in the surface layers of the
epithelium. The basement membrane of the epithelium in most cases retains its usual size, but in some
patients it may be thickened and sclerosed.
Along with pronounced dystrophic-necrotic changes in the epithelium, vascular hyperemia is noted, in all
cases the number of papillae is significantly increased. In the thickness of the epithelium and in the
subepithelial layer, focal (usually perivascular), and sometimes diffuse lymphoplasmocytic infiltrates with
an admixture of single eosinophils and polynuclear neutrophils are detected. In a small percentage of cases,
signs of active inflammation are not detected histologically. At the same time, the esophageal mucosa is
marked by an overgrowth of loose, and sometimes dense fibrous connective tissue (sclerosis). Fibroblasts
and destroyed macrophages are often found in the fields of sclerosis. Smooth muscle cells of the mucosal
lamina proper show signs of severe dystrophy or atrophy, and in rare cases a state of coagulation necrosis.

Histological examination may reveal metaplasia of the flat non-keratinizing epithelium of the esophagus,
which leads to the development of cylindrical epithelium with fundal glands (parietal, main and additional
cells in the glands are detected, and the integumentary epithelium forms typical rollers covered with
integumentary-pit epithelium). At the same time, the glands are not numerous, "squeezed" by connective
tissue growths and diffuse lymphoplasmocytic infiltrate.

If metaplasia leads to the development of cylindrical epithelium of the cardiac or fundal type of the gastric
mucosa, then the risk of developing esophageal adenocarcinoma does not increase. However, if metaplasia
leads to the appearance of specialized small intestinal cylindrical epithelium, the risk of malignancy
becomes clear. Specialized cylindrical epithelium is diagnosed as incomplete small bowel metaplasia with
the presence of goblet cells. The morphological substrate of NERD can be considered the expansion of
intercellular spaces in the basal layer of the epithelium of the esophageal mucosa, which is clearly
determined by electron microscopy.

Manometry

The study of the motor function of the esophagus allows you to study the indicators of movement of the
esophageal wall and the activity of its sphincters. In GERD, manometric examination reveals a decrease in
the pressure of the lower esophageal sphincter, the presence of a hiatal hernia, an increase in the number of
transient sphincter relaxes, and a decrease in the amplitude of peristaltic contractions of the esophageal wall.

pH-metric examination of the esophagus

The main method for diagnosing GERD is pH-metry.

The study can be performed both on an outpatient basis and in an inpatient setting. When diagnosing GERD,
the results of pH-metry are evaluated by the total time during which the pH takes values less than 4 units,
the total number of refluxes per day, the number of refluxes lasting more than 5 minutes, and the duration of
the longest reflux.

Daily pH measurement has a very high sensitivity (88-95 %) in the diagnosis of GERD and also helps in the
individual selection of medications.

X-ray examination

X-ray examination of the esophagus can be used for screening diagnosis of GERD and can detect hiatal
hernias (contrast examination is performed in the Trendelenburg position), esophageal strictures, diffuse
esophagospasm, and gastroesophageal reflux.

In the diagnosis of GERD, such methods as bilimetry, scintigraphy, and the Bernstein test can be
used. Bilimetry allows you to verify alkaline (bile) refluxes, scintigraphy reveals violations of the
motor-evacuation function of the esophagus. The Bernstein test consists of injecting 0.1 N HCl solution into
the esophagus, which leads to typical clinical symptoms in GERD. The introduction of chromoendoscopy
helps to detect metaplastic and dysplastic changes in the esophageal epithelium by applying substances to
the mucous membrane that color healthy and affected tissues differently.

Endoscopic ultrasound examination of the esophagus is the main technique for detecting endophytic
growing tumors.

GERD should be included in the differential diagnostic search for patients with chest pain, dysphagia,
gastrointestinal bleeding, or bronchial obstructive syndrome.

Treatment of GERD

Treatment goals: relief of clinical symptoms, healing of erosions, prevention or elimination of

complications, improvement of quality of life, prevention of relapse. Currently, the main principles of
GERD treatment can be considered as follows: the need to prescribe large doses of antisecretory drugs and
conduct long-term basic (at least 4-8 weeks) and maintenance (6-12 months) therapy. If these conditions are
not met, the probability of relapse of the disease is very high. Studies conducted in many countries around
the world have shown that more than 80% of patients who do not receive adequate supportive treatment will
relapse within the next 26 weeks, and within a year the probability of relapse is 90-98%. This implies the
mandatory need for maintenance treatment.

Lifestyle changes should be considered a prerequisite for effective anti-reflux treatment of patients with
GERD. First of all, it is necessary to eliminate smoking and normalize body weight.

You should avoid eating sour fruit juices, foods that increase gas formation, as well as fats, chocolate,
coffee, garlic, onions, peppers, tomatoes. It is necessary to exclude the use of alcohol, very spicy, hot or cold
food and carbonated drinks. Take food often (4-5 times a day), in small portions and chewing thoroughly.

Patients should avoid overeating; they should stop eating at least 3 hours before bedtime. You can not wear
tight belts, work in a slope. Sleep with the head end of the bed raised. Patients should be warned about the
side effects of drugs that reduce the tone of the lower esophageal sphincter (theophylline, progesterone,
antidepressants, nitrates, calcium antagonists), and can also cause inflammation (nonsteroidal
anti-inflammatory drugs, doxycycline, quinidine).

Drug treatment includes well-known groups of drugs. Antacids are effective in treating moderate to rare
symptoms, especially those associated with non-compliance with the recommended lifestyle. Antacids
(almagel, maalox, gastal, rutacid) should be taken frequently (depending on the severity of symptoms),
usually 1.5-2 hours after meals and at night. Antacids, creating a thick foam on the surface of the stomach
contents with each episode of reflux, return to the esophagus, having a therapeutic effect. The effect of
antacids is twofold: first, due to the content of antacids, they have an acid-neutralizing effect, and, secondly,
when they enter the esophagus, they form a protective film that creates a pH gradient between the mucous
membrane and the lumen of the esophagus and protects the mucosa from the aggressive influence of gastric
juice.

Prokinetics restore esophageal motility: they increase the tone of the lower esophageal sphincter, increase
esophageal motility and improve esophageal clearance.

Prokinetic drugs such as domperidone and itopride are considered pathogenetic treatments for GERD, as
they normalize the motor function of the upper digestive tract, restore active gastric motility, and improve
antroduodenal coordination. Prokinetics are prescribed at a dose of 10 mg (domperidone) or 50 ml (itopride)
3 times a day 30 minutes before meals.
Prokinetics are effective only in the complex therapy of erosive esophagitis together with proton pump
inhibitors (PPIs).

In the presence of erosive esophagitis, it is necessary to prescribe PPIs that very effectively control the pH
level in the lower third of the esophagus. Due to a decrease in the time of contact of hydrochloric acid with
the esophageal mucosa, the severity of the symptoms of the disease decreases and they quickly disappear
(within 3 days when omeprazole and esomeprazole are prescribed at a dose of 40 mg and during the first day
when rabeprazole is prescribed at a dose of 20 mg). This powerful inhibition of acid production is the main
factor contributing to the healing of erosive and ulcerative lesions of the esophageal mucosa in patients with
GERD. The use of PPIs should be the means of choice for the treatment of severe esophagitis. The course of
treatment for any of the PPIs should be at least 8 weeks (in the presence of stage 2 or more severe
esophagitis according to the Savary-Miller classification) and at least 4 weeks in the presence of stage 1
esophagitis. In the treatment of NERD, PPIs are used in half a dose (omeprazole group drugs-at a dose of 20
mg, rabeprazole-at a dose of 10 mg), and in the treatment of NERD, it is possible to use PPIs "on demand"
(when symptoms appear).

If heartburn rarely occurs and does not last for a long time, or if there is no history of erosive esophagitis, we
can recommend taking one of the PPIs in the "on-demand" mode, that is, only if complaints occur
(rabeprazole at a dose of 10 mg, omeprazole 20 ml, esomeprazole 10 mg, pantoprazole 20 mg, lansoprazole
30 mg 1-2 times a week, but at least once in 4 weeks). However, if these patients are obese, have a hiatal
hernia, or if heartburn occurs more often than 3 times a week, a constant intake of PPIs (rabeprazole 20 mg,
omeprazole 20 mg, esomeprazole 10-20 mg, pantoprazole 20-40 mg, lansoprazole 30 mg 1 time a day for 4
weeks) should be prescribed.

In the presence of isolated erosions of the esophagus (stage 1), the probability of their healing within 4
weeks of PPI treatment is high. Therefore, the main course in this case can be only 4 weeks (rabeprazole at a
dose of 20 mg 1 time a day, and omeprazole 20 mg, esomeprazole 10-20 mg, pantoprazole 20-40 mg,
lansoprazole 30 mg-2 times a day) with a control endoscopic examination. If multiple erosions of the
esophagus (stages 2-4 of esophagitis) are detected, as well as complications of GERD, the course of
treatment with any drug from the PPI group should be at least 8 weeks, since with this duration of therapy,
90-95% of the effectiveness can be achieved. With a 4-week course of treatment with any PPIs, the healing
rate of multiple esophageal erosions is significantly lower. In addition, such an unjustified reduction in the
duration of treatment of erosive forms of GERD can cause rapid subsequent relapse, as well as the
development of complications.

H Blockers2- histamine receptors (ranitidine, famotidine) can also be used to reduce the acidity of gastric
juice, but they are less effective than PPIs.

When reflux esophagitis is caused by the throwing of bile into the esophagus, ursodeoxycholic acid is
prescribed at a dose of 250 mg / day in combination with prokinetics.

Maintenance therapy after erosion healing should be performed for 16-24 weeks. In this case, both full and
half doses of PPIs can be used. So, after healing of single erosions of the esophagus after a 4-week course,
as well as successful healing of multiple erosions after an 8-week course, you can prescribe PPIs 1 time a
day (rabeprazole at a dose of 10 mg, omeprazole 20 ml, esomeprazole 10 mg, pantoprazole 20 mg,
lansoprazole 30 mg), including in the following cases: in "on demand" mode. If there are complications of
GERD, maintenance therapy should be performed with a full-dose PPIs.

Patients with GERD are subject to active medical supervision with a control examination conducted at least
once a year. In the presence of complications, it is necessary to examine such patients 2 times a year,
including with the use of endoscopic examination.
The highest percentage of effective treatment of GERD exacerbations and maintenance of remission is
achieved with the combined use of PPIs and prokinetics. In the presence of alkaline (bile) reflux, large doses
of enveloping drugs should be added to the combination of PPIs and prokinetics.

Patients whose clinical symptoms of the disease are not accompanied by the development of esophagitis
need to take medications in the "on-demand" mode. However, patients with erosive-ulcerative esophagitis
with this maintenance regimen will still have a high risk (80-90%) of developing a relapse of the disease
within a year. The likelihood of relapses increases in cases of resistance of the initial stages of esophagitis to
therapy with antisecretory drugs, as well as when low pressure in the lower esophageal sphincter is
detected. Such patients require the use of high doses of antisecretory drugs.

The decision on the duration of maintenance therapy for GERD should be made taking into account the
patient's age, the presence of concomitant diseases, existing complications, as well as the cost and safety of
treatment. Antireflux surgical treatment is considered indicated for a complicated course of the disease
(repeated bleeding, peptic strictures of the esophagus, development of Barrett's syndrome with high-grade
epithelial dysplasia), as well as for proven ineffectiveness of drug therapy. The question of surgical
treatment should be considered together with an experienced surgeon in this field, if long-term conservative
treatment of GERD, which was carried out very actively, was unsuccessful, all measures were taken to
normalize the lifestyle and the presence of pronounced gastro-esophageal reflux was proved (using
pH-metry).

Management of patients with Barrett's esophagus

The need for active dispensary monitoring of patients with Barrett's esophagus is due to the possibility of
preventing esophageal adenocarcinoma in cases of early diagnosis of epithelial dysplasia. Verification of the
diagnosis of Barrett's esophagus and determination of the degree of dysplasia is carried out by histological
examination. If low-grade dysplasia is detected, it is necessary to prescribe rabeprazole at a dose of at least
20 mg per day – or omeprazole group drugs at a dose of at least 40 mg per day, with a repeat of the
histological examination after 3 months. If low-grade dysplasia persists, patients are recommended to
continue the constant use of PPI at the same dose and conduct a histological examination after 3 and 6
months. Then a histological examination is performed annually. If a high degree of dysplasia is detected,
rabeprazole should be prescribed at a dose of at least 40 mg per day, and omeprazole, esomeprazole,
pantoprazole-40 mg 2 times a day, with a parallel assessment of the results of histological examination and
subsequent decision on endoscopic or surgical treatment of the patient.
Differential diagnosis and Diseases that manifest as diarrhea (gastrointestinal tumors, inflammatory
treatment of intestinal bowel diseases, mono-and disaccharidase malabsorption, celiacdisease,
dyspepsia. functional disorders, infectious diseases), differential diagnosis.
Malabsorption syndrome.
Irritable bowel syndrome.
Differential diagnosis of diseases associated with constipation (dilatation
of the colon, overgrown colon syndrome, colon tumors, diverticula,
distalcolon disease, irritable bowel syndrome). Diagnostic capabilities
(X-ray contrast examination of the intestine, examination of feces,
enzymes, endoscopic methods, biopsy of the intestinal mucosa).

DIFFERENTIAL DIAGNOSIS AND TREATMENT OF INTESTINAL

DYSPEPSIA SYNDROME
Intestinal dyspepsia is characterized by splashing, rumbling in the abdomen, localized mainly in
the middle and lower parts of it, flatulence, increased gas production (flatulence), diarrhea,
constipation or alternating them. The pain syndrome is usually not clearly expressed and is caused by
flatulence, spastic phenomena.
Diarrhea (diarrhea) – frequent (more than 2 times a day) discharge of liquid feces, associated
with accelerated passage of contents through the intestines, impaired absorption of water and
electrolytes, and increased mucus formation. There is a distinction between acute diarrhea, which
occurs suddenly and lasts up to two weeks, and chronic diarrhea, which lasts for more than two weeks
or has a recurrent course.
Diagnostic search is based on the principle of dividing diarrhea syndrome into two groups –
infectious and non-infectious origin. This is the first question that a doctor should decide when
performing a differential diagnosis. No less important is the isolation of diarrhea in the form of a
monosymptome that does not determine the severity of the underlying disease, or vice versa – as a
leading clinical syndrome with its own characteristic features, requiring special laboratory diagnostics,
as well as differentiated etiotropic and pathogenetic therapy.
Acute diarrhea with a sudden onset, occurring in previously healthy people, is usually infectious
in nature. The infectious nature of diarrhea is supported by epidemiological history data: eating food
prepared in violation of sanitary and technological conditions, drinking water from unverified sources,
non-compliance with personal hygiene rules, the presence of patients with intestinal diseases in the
family, at work. Infectious diarrhea is accompanied by fever, headache, anorexia, vomiting, malaise,
and myalgia. Its etiology can be viral, bacterial, or protozoal. At the initial stages of diagnosis, it is
difficult to establish the etiological diagnosis of a sporadic case of diarrheal disease. In this situation,
it is most justified to make a syndromic diagnosis that reflects the predominant lesion of one or
another part of the gastrointestinal tract. In this regard, the most commonly used formulations are
gastroenteritis, enteritis, enterocolitis, colitis and gastroenterocolitis. Enteritis is manifested by
rumbling and" transfusion " in the abdomen, often audible and at a distance, periodic pain throughout
the abdomen or in the navel, imperative urges to defecate, abundant infrequent loose stools. Bowel
movements are watery, with lumps of undigested food due to a violation of enzymatic processes and
absorption in the small intestine. The color of feces is light, golden-yellow or greenish due to the
presence of unchanged bile pigments, increased peristalsis and rapid movement of intestinal contents.
In severe acute enteritis, the bowel movements may have the appearance of a translucent whitish
cloudy liquid with flocculent or pityritic suspended particles, which form sediment after settling. On
palpation of the abdomen, rumbling, " splashing noise" along the small and large intestines are noted,
the small intestine is not infiltrated. For diseases in which enteritis is the main syndrome, the
development of dehydration is characteristic. Colitis is characterized by periodic cramping pains in the
lower abdomen, more often in the left iliac region, false urges to defecate, tenesmus, and a feeling of
incomplete bowel release after defecation. Typical features of the coptic syndrome are the
homogeneous nature of bowel movements, their mushy or semi-liquid consistency, and the presence
of pathological impurities such as mucus, blood, and pus. With severe colitis, accompanied by
frequent stools, discharge becomes more and more scarce with each defecation, losing the fecal
character. When a hemorrhagic process develops in the terminal parts of the colon, the stool consists
of only mucus with streaks of blood ("rectal spittle"). When hemorrhages and necrosis are primarily
located in the right half of the colon, the mucus is uniformly colored red or brown- red ("raspberry
jelly"). Pus in its pure form (without mucus) in the acute period of the disease is almost never
observed. It can be detected during the period of convalescence in the last portions of bowel
movements or on the surface of the formed feces, which is almost impossible. it always indicates a
persistent focal inflammatory or ulcerative process in the rectum and sigmoid colon. Scarlet blood in
the stool may appear due to bleeding from hemorrhoidal veins, anal fissures, ulcers, polyps, and a
decaying tumor of the lower colon. In these cases, the blood is not mixed with feces, is on
the surface, often in the form of individual drops, sometimes clots, mucus and pus are absent or
found in very small amounts. Palpation of the large intestine has the character of a dense rigid tube,
tonic shortens, becomes less mobile.
Acute diarrhea of suspected viral etiology typically lasts 1-3 days and is characterized by a
small intestinal origin. The intestinal mucosa is not affected by viral diarrhea. A transient syndrome
of impaired absorption of fats and xylose is detected.
Bacterial diarrhea can be suspected if cases of simultaneous development of a similar disease in
several people who consumed the same food are established. If diarrhea develops within 1-3 (up to 6)
hours after eating, it is most likely that it is caused by ingestion of a previously ingested toxin (most
often a staphylococcal exotoxin) – food toxicoinfection. The clinic is dominated by intoxication,
abdominal pain. The disorder of the stool is not observed constantly. There is a short-term diarrhea
with a stool frequency of 1-5 times a day without characteristic pathological admixtures, which stops
as the patient's general condition stabilizes .
If there is a latent period of 12-24 hours after eating contaminated food, salmonellosis can be
assumed. Severe intoxication, febrile fever, pain in the epigastrium and around the navel, repeated
vomiting, profuse fetid stool of the color of "swamp mud" are characteristic. The diagnosis is verified
by salmonella discharge from vomit, gastric lavage, and feces.
Symptoms of intoxication and pain are atypical for cholera. To the fore comes a plentiful,
watery stool, which quickly loses its fecal character, acquiring the appearance of " rice broth", without
smell. Possible vomiting. Symptoms of dehydration and electrolyte metabolism disorders (convulsive
muscle contractions) often develop. The diagnosis is verified using bacteriological research methods.

3.1. Dysentery is a classic representative of acute colitis. The collection period is 2-3 days.
Intoxication is moderate, with recurrent pain in the lower abdomen, more often in the left iliac region,
which is accompanied by the urge to defecate. Stool is not plentiful, frequent, with an admixture of
mucus and streaks of blood ("rectal spitting"), tenesmus, a feeling of incomplete release of the
intestine after defecation. Dehydration, as a rule, does not happen. Verification is bacteriological.
 3.2. Amoebiasis or amoebic dysentery occurs mainly in the summer and autumn period.
The beginning is gradual, the stool is 3-5 times a day, mushy, retains a fecal character, often with a
large amount of sticky mucus, stained with blood (a symptom of "raspberry jelly"). Abdominal pain
is moderate, intoxication is mild. On palpation- compaction and tenderness of the caecum, the
ascending colon may be involved. Who can increase the liver. During colonoscopy ulcers filled with
purulent detritus and bleeding on contact with the colonoscopy are found against the background of
an intact mucosa of the right parts of the large intestine. The diagnosis is verified when a vegetative
form of histolytic amoeba is detected in the feces.
Other causes of acute diarrhea may include various types of intoxication, as well as food
allergies.
The approach to the diagnosis of acute diarrhea depends on the clinical situation. It is considered
reasonable to refrain from conducting any diagnostic tests in cases of mild diarrhea that is not
accompanied by any complications, which are considered as a special case of an epidemic viral
disease. In cases of severe diarrhea or if there is a suspicious epidemiological history, a
bacteriological examination of stool cultures with microscopy is necessary to detect parasites and
inflammatory cells. Proctosigmos copy is usually performed in patients with bloody diarrhea and in
those patients who do not improve their condition within10 days. In case of a large loss of fluid, the
electrolyte content in the blood serum is examined to determine the need for replacement therapy. If
the bacterial nature of diarrhea is confirmed, specific antibacterial therapy is performed in
combination with detoxification and, if necessary, rehydration.

3.3. Chronic diarrhea that lasts for several weeks (permanent or intermittent) can be a
functional symptom or manifestation of a serious disease. With the predominance of fermentation
processes in the intestines, the reaction is sharply acidic compared to the release of foamy light
yellow is pscontaining abundant phosphophilic flora, indigestible fiber and starch. Putrefaction
processes are accompanied by liquid, dark-colored expectorations of a sharply unpleasant smell, an
alkaline reaction. They contain a lot of muscle fibers, an increased content of nitrogen, ammonia,
indole, skatole, and other products of incomplete protein breakdown.
In the differential diagnosis of chronic diarrhea, it is necessary to keep in mind a wide range of
diseases, starting with the pathology of the intestine itself, other organs of the gastrointestinal tract,
as well as diseases that are not directly related to the gastrointestinal tract.
1. Intestinal diseases.
1.1. Chronic enteritis
1.2. Chronic colitis
1.3. Crohn's disease
1.4. Non-specific ulcerative colitis
1.5. Ischemic colitis
1.6. Diverticular disease
1.7. Eosinophilic gastroenteritis
1.8. Intestinal dysbiosis
1.9. Intestinal tuberculosis
1.10. Whipple's disease
2. Intestinal tumors
2.1. Carcinoid
2.2. Lymphoma
3. Congenital enzymopathies
3.1. Lactase deficiency
3.2. Gluten-free enteropathy
4. Stomach diseases
 4.1. Gastritis with achilles
4.2. Disease of the operated stomach (dumping syndrome)
4.3. Stomach cancer
5. Diseases of the pancreas
5.1. Chronic pancreatitis
5.2. Tumors
5.3. Zollinger-Ellison syndrome
6. Diseases of the endocrine system
6.1. Thyrotoxicosis
6.2. Diabetes mellitus
6.3. Addison's Disease
6.4. Hypoparathyroidism
7. Systemic scleroderma
8. Metabolic diseases (amyloidosis, hypovitamiosis)
9. Gynecological diseases (endometriosis, plastic cicatricial peritonitis).

3.3.1. Chronic enteritis – is an inflammatory and dystrophic disease of the small

intestine, characterized by the development of atrophy and sclerosis of the mucous
membrane, a violation of its main functions – digestion and absorption, resulting in
secondary metabolic and immune disorders. The causes of primary damage to the small
intestine can be bacteria, viruses, giardia, helminths, pathogenic fungi (if there is an
inadequate immune response leading to chronization of the process). Non-infectious
factors: overeating, unbalanced nutrition in protein and vitamins, abuse of refined foods,
carbohydrates, and salt; exposure to toxic substances (lead, arsenic), medications
(salicylates, non steroidal anti-inflammatory drugs, cytostatics, uncontrolled use of
antibiotics, sedatives). Morphologically, chronic enteritis is manifested by inflammatory
and dystrophic changes in the mucosa of the small intestine, with progressive
process-atrophy and sclerosis. The entire small intestine or its parts are
affected-duodenitis, eunitis, ileitis. The clinical picture of chronic enteritis consists of two
symptom complexes: a local enteral syndrome caused by a violation of the esophageal
processes, and a symptomcomplex associated with a violation of the absorption of food
ingredients, which causes disorders of all types of metabolism and changes the
homeostasis of the organ (general enteral syndrome). Local enteral syndrome is
manifested by a symptom complex of intestinal dyspepsia: bloating mainly in the
paraumbilical region, loud rumbling, abdominal transfusion, diarrhea, less often unstable
stools. Stool in enteritis is plentiful (feces), but not too frequent (up to 3-8 times a day),
often in the evening and at night. Pheasants are light yellow in color, sometimes have a
clay appearance, as a rule, without admixture of blood. Diarrhea and flatulence increase in
the second half of the day (at the height of digestion), often accompanied by a feeling of
fullness, heaviness and abdominal pain, mainly in the mesogastrium and the umbilical
region. Palpation of the abdomen reveals: pain in the parotid region, as well as on the left
in the mesogastrium at the level of XII thoracic - I lumbar vertebra (Porges ' symptom),
"splashing noise", rumbling in the caecum (Obraztsov's symptom). General enteral
syndrome is characterized primarily by a disorder of protein metabolism due to a decrease
in the activity of proteinases in the mucosa of the small intestine, which leads to a
violation of the cleavage and absorption of food protein substrates. Violation of protein
metabolism is manifested by hypoproteinemia with hypoalbuminemia, hypoproteinemic
edema, dystrophic changes in internal organs andsystems, and progressive weight loss.
Violation of carbohydrate metabolism is less common, but a decrease in the activity of
intestinal gamma-amylase, lactase, maltase, invertase leads to a change in the hydrolysis of
starch, disaccharides, manifested by intolerance to milk, sugar, the development of
fermentation dyspepsia, hypoglycemic states during physical exertion, and weight loss
progresses. The disorder of lipid exchange is indicated by steatorrhea (fatty acids, soaps in
feces), a decrease in cholesterol, phospholipids in blood serum, as well as lipids in bile, and a
violation of the absorption of fat-soluble vitamins (D, A). The formation of insoluble calcium and
magnesium salts of fatty acids is associated with a change in calcium absorption, which manifests
itself as appositive symptom of muscle roll, convulsions that periodically occur in "unmotivated"
bone fractures, osteoporosis, and increased excitability. Chronic enteritis shows a decrease in the
content of potassium in plasma, red blood cells and intestinal juice , and an increased content of
sodium in both в plasma and в red blood cells. Clinical picture: weakness, rapid fatigue, muscle
pain, nausea, vomiting, extrasystole, hypotension, impaired renal function. There are also disorders
in the metabolism of magnesium, phosphorus, and trace elements, as evidenced by a decrease in
their concentration in the blood and urine, and increased excretion with feces. The consequence of
impaired absorption is iron deficiency, often combined with folic acid and vitaminB12deficiency,
which manifests itself in progressive anemia. There are signs of polyhypovitaminosis (deficiency
of vitamins C,B2,B6,B1, K, A, D, E). The clinical picture often includes glossitis, angular stomatitis,
cheilitis, irritability, loss of appetite, drowsiness, seborrheic dermatitis of the face, hair loss, dry
throat, dysphagia, twilight vision disorders, and increased bleeding. There are signs of dysfunction
of the pituitary gland, adrenal glands, sex glands, and thyroid gland. Often, chronic enteritis
develops metabolic hepatitis, pancreatitis, colitis, and myocardial dystrophy. The general blood test
reveals micro-and macrocytic anemia, increased ESR; in the coprogram-steatorrhea (fatty acids
and soaps), creatorrhea, amylorrhea. Bacteriological examination of feces reveals a decrease or
complete absence bifidumbacteria, conditionally pathogenic flora is actively growing. In the blood
serum: hyperkinemia, hypoalbuminemia, hypocalcemia, hypocalemia, hyponatremia,
hypoferremia, hypocholesterolemia, a decrease in the content, beta - lipoproteins, glucose is noted.
To study the absorption capacity of the small intestine, a D-xylose test is performed, and a Shilling
test or a vitamin B12 absorption test is used to assess the function of the ileum. In order to
diagnose exudative enteropathy syndrome, enteral protein loss is determined using
131
131I-polyvinylpyrrolidine. A violation of the digestion and absorption of lipids is judged by
determining their losses with feces (by the radioisotope method). In order to diagnose
disaccharidase deficiency, as well as bacterial contamination of the small intestine, a hydrogen test
is used. X-ray examination (enterography) allows us to clarify the topography, as well as changes
in mucosal relief, and assess motor transport function. FGDS and histological examination of
biopsies can detect atrophic duodenitis, the diagnosis is clarified by histomorphological
examination of the biopsy of the small intestine mucosa. Treatment: diet No. 4, which helps to
reduce inflammation, fermentation processes and hyperexudation in the intestines, and normalize
intestinal motility. Antibacterial therapy is prescribed taking into account the nature of dysbiosis
(see Intestinal dysbiosis). At the end of the course of antibacterial therapy, bacterial preparations
are indicated: bifidumbacterin, lactobacterin, complex preparations (omniflor, omnifloral, linex).
To stop diarrhea-loperamide (imodium) 2 capsules in the morning and 1 capsule after stools, but
not more than 6 capsules per day; astringents and adsorbents-de-nol 1 tablet 4 times a day, white
clay up to 12 g per day, decoctions and infusions of medicinal plants (alder cones, bark oak,
pomegranate rind, roots and rhizomes of blood, serpentine, cinquefoil prunus, St. John's wort
flowers, horse sorrel root, knotweed, sage leaf, marshmallow root, dried blueberries). To normalize
the digestive processes, various preparations are used: pancreatin 1-2 g 4 times a day, mezim-forte,
2 tablets 4 times a day. Enzyme preparations should be taken with meals, the course of treatment is
1.5-2 months, and sometimes longer. With severe flatulence, polyphepan is indicated for 1
tablespoon3 times a day, activated charcoal (the course of treatment is 10-14 days). In chronic
enteritis with protein deficiency, parenteral administration of albumin (200-400 ml of 20 %
solution), plasma ( 200-400 ml each) is necessary. At the same time, anabolic drugs are also
prescribed: retabolil 1 ml of a 5% solution intramuscularly 1 time in 10 days, nerobol по 0.005 g
2-3 times a day (the course of treatment is 3-4 weeks). To correct the water - electrolyte balance,
the following drugs are indicated: panangin, calcium gluconate, 10 ml of a 10 % solution in 250
ml of 5% glucose solution or isotonic sodium chloride solution for 2-3 weeks in a vein drip. When
metabolic acidosis occurs, 200 ml of a 4% sodium bicarbonate solution, 1.5 g of magnesium
sulfate in 500 ml of an isotonic solution of sodium chloride are additionally injected into the vein
dropwise. In metabolic alkalosis, potassium chloride, 2-4 g, calcium chloride, 3 g, and magnesium
 sulfate, 1-2 g are administered in 500 ml of an isotonic sodium chloride solution. At the same time,
it is necessary to prescribe vitaminsb1,B6,B12, riboflavin, folic acid, nicotinic acid, vitamin E, which
are prescribed in the usual pharmacopoeial doses. Iron preparations are indicated for iron
deficiency anemia: ferroplex 2 tablets 3 times a day, the course of treatment is up to 3-6 months.
Mineral waters for chronic enteritis should be taken with caution (in the absence of diarrhea), in a
warm form, without gas, no more than 1/4/4-1/3/3 cup per reception. Only slightly mineralized waters
can be recommended : Slavyanovskaya, Smirnovskaya, Yessentuki-4, Izhevsk, Narzan. The time
of their intake depends on the state of the acid -forming function of the stomach: with reduced acid
production – 15-20 minutes, with preserved – 40-45, and with increased- 1.5 hours before meals.
From physiotherapy procedures, DMV therapy, paraffin applications, electrophoresis of vocaine,
zinc on the mesogastric region are used.

3.3.2. Chronic colitis is a morphologically confirmed inflammatory or dystrophic

process that affects the entire colon (pancolitis) or its divisions (segmental colitis).

Etiology. Bacterial infection (shigella, salmonella, campylobacter, yermidia, clostridium, etc.),

while the causative agent of the disease may no longer be detected, but after treatment from
an acute disease, changes in the motor and enzymatic function of the intestine remain,
dysbacteriosis develops, the structure of the mucous membrane changes, which contributes
to the chronization of the process. Helminths, opportunistic flora and protozoa (amoebae,
giardia, Trichomonas, balantidia). Alimentary reasons: violation of the diet, monotonous,
containing a large amount of carbohydrates or proteins, a diet devoid of vitamins, frequent
use of hard-to-digest fiber and spicy foods, alcohol abuse. Exogenous (poisoning with
mercury, lead, phosphorus, arsenic compounds) and endogenous intoxications (with uremia,
liver failure, hyperthyroidism, Addison's disease, gout). Intestinal dysbiosis, radiation
exposure (radiation therapy), adhesions in the abdominal cavity, megacolon, diverticular
disease, coprostasis with persistent constipation, abuse of laxatives and cleansing enemas
contribute to the appearance of the inflammatory process. There are "drug-induced colitis"
that develop with prolonged uncontrolled use antibiotics, laxatives and choleretics,
enveloping and absorbing antacids, sequestrants, salicylates, digitalis preparations, and
others. Clinical manifestations: aching, bursting pain, sometimes paroxysmal, appearing or
increasing in 30-90 minutes after eating, before defecation. It is localized in the
hypogastrium, along the flanks, but can be diffuse (without a clear localization), often
radiates to the back, to the anus, and decreases after defecation and gas discharge. When the
pathological process spreads to the serous lining of the intestine (pericolitis) or regional
lymph nodes (mesadenitis) the pain becomes constant, monotonous, it is not associated with
food intake, but increases when driving, shaking, jumping, as well as after defecation,
cleansing enemas, with active heat treatment (mud, diathermy, paraffin), from a hot water
bottle. Constipation or diarrhea, as well as their occurrence (unstable stools), the urge to
defecate immediately after eating (increased gastrointestinal reflex), and sometimes during
sleep ("wakeup" symptom), a feeling of incomplete bowel movement after defecation. There
may also be so-called "constipation diarrhea", when constipation is replaced by profuse once
or twice diarrhea, and then constipation is again noted for several days. Flatulence – bloating
spreading mainly to the lower and lateral parts of the stomach, accompanied by a feeling of
heaviness, rumbling, transfusion in the abdomen. Weight loss in colitis, as well as anemia,
hypovitaminosis, is more often explained by an exaggerated diet and dysbiosis that develops as a
result of uncontrolled use of antibiotics. In the absence of tidal damage to the colon, the clinical
manifestations of chronic colitis are associated with the localization of the pathological process:
tiflitis, transversitis, sigmoiditis, proctosigmoiditis. With typhitis or right-sided colitis, diarrhea is
more often observed, sometimes up to 10 times a day, or alternating diarrhea with short-term
constipation; pain in the right half of the abdomen, especially in the right abdominal region, often
radiating to the groin, leg, and lower back. Palpation reveals spasm or expansion of the cecum,
restriction of its mobility in peritiflitis, and soreness. Transversitis-a lesion of the transverse colon-is
rarely observed independently, more often with pancolitis. He is characterized by pain, rumbling,
distension in the middle part of the abdomen, appearing immediately after eating, alternating diarrhea
and constipation. Deep palpation reveals a painful, swollen gas or spasmodic transverse colon.
Sometimes spasmodic areas alternate with expanded ones, in which dense contents and rumbling are
noted. I solated lesion of the splenic bend of the colon (angulitis) is more common than it is
diagnosed, especially in left-sided colitis. Severe pain in the left hypochondrium is characteristic,
often radiating to the back and left half of the chest. There are also unstable stools, loud rumbling in
the left hypochondrium, often preceding loose stools. Percussion reveals tympanitis in the upper left
quadrant of the abdomen, while palpation reveals pain in the same area. Left-sided colitis (proctitis,
sigmoiditis, proctosigmoiditis) is most common. The main signs of this form of the disease are pain
in the left iliac region, as well as in the rectum, a feeling of pressure and bursting in the
mesogastrium, which increases after defecation, stool discharge, false urges with the discharge of
gases, sometimes mucus. The stool is mushy or liquid, heterogeneous, in small portions several times
a day. Frequent sphincteritis, cracks, hemorrhoids. On palpation, the sigmoid colon is enlarged,
swollen with gases, and painful. It can detect dense fecal masses, which gives the intestine a bumpy
appearance and sometimes requires the exclusion of the tumor process. The diagnosis of chronic
colitis is based on anamnestic, clinical data, results of coprological and bacteriological examination
of feces; it is confirmed by irrigation, rectoromanoscopy, colonoscopy with mucosal biopsy and
morphological examination of biopsies, and ultrasound of the colon. Treatment. Diet (46), frequent,
fractional meals (5-6 times a day). Patients with severe constipation are recommended to eat foods
that contain a sufficient amount of fiber and dietary fiber: beets, carrots, pumpkins, zucchini,
jerusalem artichoke, prunes, apricots, wheat bran, as well as vegetable and fruit juices. With apositive
bacteriological analysis of feces, antibacterial therapy is performed according to the same principles
as for enteritis. When diarrhea is prescribed astringent, enveloping and absorbing drugs: de-nol,
tanalbin (1 g 3 times a day), white clay (1-2 g 4-6 times a day). Carbolene, polyphepane, activated
charcoal, and an infusion of chamomile flowers, листьев mint leaves, плодов cumin, dill, and fennel
are indicated for flatulence. Normalization of the motor-evacuation function of the intestine can
contribute to cerucal, domperidone (motilium). Use microclysters with antipyrine (0.5 g) and
anesthesin (0.3 g), novocaine (20 ml of 0.25 % solution or sea buckthorn oil (30 ml), rosehip (30 ml);
candles "Anestezol", "Neoanuzol", rectal tampons with solcoseryl, pelloidin. Among physiotherapy
procedures, warming compresses (water, semi– alcohol, oil) are recommended during exacerbation,
and mud, ozokerite, paraffin, diathermy, and warm bathsare recommended during remission.
Electrophoresis with novocaine, platifillin, calcium chloride, as well as UHF and ultrasound is
widely used. Spa treatment is indicated only during remission (Krinitsa, Bobruisk, Naroch, Porechye,
Yessentuki, Zheleznovodsk, Druskeninkai).

3.3.3. Non-specific ulcerative colitis (ulcerative colitis, hemorrhagic rectitis, recto–

colitis) is a chronic recurrent ulcerative-necrotic inflammation of the colon mucosa of a
non-specific nature. The etiology of the disease remains unclear. UA should most likely be
considered as the result of immune (autoimmune) reactions in an organism sensitized to
various antigens, mainly of intestinal origin. The pathological process begins, as a rule, in
the rectum and, spreading in the proximal direction, can acquire a total character.
Clinical picture. The beginning is gradual, bothered by constipation, unpleasant
sensations during defecation. In 1/3/3, there is an admixture of blood in the stool. There
may also be a "dysentery-like" onset of the disease: diarrhea with blood, fever,
intoxication. Such an onset is an acute form of deficiency, in which a detailed picture of
the disease is already formed by the 3rd-5th day. Extra-intestinal symptoms – joint pain,
low-grade fever. In the advanced stage, bleeding is the leading symptom. Blood loss with
feces can be different: from a strip on toilet paper to 10-15 ml per defecation. Heavy
(profuse) bleeding is also possible. The blood is red, mixed with feces. The second
characteristic symptom of ulcerative colitis is frequent loose stools with an admixture of
mucus and pus. The frequency of stool in patients is 3-4 times a day, and in severe
cases-up to 20%. Often, in an imperative pose, only bloody mucus is released on to the
chair. Abdominal pain is a secondary symptom, in a pronounced stage it is observed in 2/3/3
of patients. Most often, they are cramping and localized in the left iliac region or in the
hypogastrium. Tenesmus is quite common. The general condition suffers: weakness,
decreased performance, temperature reaction, headaches, insomnia, arthralgia, pronounced
symptoms of asthenia, weight loss. There are violations of protein metabolism
(dysproteinemia with hypoalbuminemia may be accompanied by edema), water-salt,
vitamin imbalance, hypochromic anemia, dystrophic changes in various organs and tissues
with the formation of intestinal dysbiosis, chronic hepatitis, pancreatitis, and myocardial
dystrophy. Pyelonephritis, nephritis, erythema nodosum, pyoderma, aphthous stomatitis,
glossitis, ocular manifestations (episcleritis, irites, uveitis) are not uncommon.
Complications of ulcerative colitis: anal fissures, perianal abscesses, inflammatory polyps
of the colon, дисбактериоз intestinal dysbiosis, which occurs in a number of patients with
septicopyemia, perforation of the colon. Perforation of colonic ulcers in UC is
distinguished by an erased clinical picture, characterized by a sudden increase in
abdominal pain, a rapid increase in intoxication, and symptoms of peritoneal irritation are
not expressed. A survey X-ray of the abdominal cavity can confirm the perforation – gas is
detected in the free abdominal cavity. Toxic dilatation is the result of toxic and immune
damage to the submucosal and intermuscular nerve plexuses, which significantly
complicates the prognosis. The patient appears or abdominal pain worsens, body
temperature rises, and vomiting occurs. Stool and gas retention develop, bloating
increases. On examination: the abdomen is asymmetrically swollen, tympanitis is detected
above the areas of swelling, peristalsis is weakened or absent. On the survey radiograph , a
sharply dilated area of the colon is visible.
Diagnostics. In the peripheral blood, leukocytosis with non-neutrophilic shift, increased
ESR, anemia; water-electrolyte disorders (reduced concentration of potassium, calcium,
less often sodium and chlorine in blood plasma); increased level α2-globulins, gamma-and
immunoglobulins, hypoproteinemia with hypoalbuminemia, hypocholerolemia are
detected. The coprogram contains blood, pus, mucus, creatorrhea, synathorrhea, and
amylorrhea, and increases the content of organic acids, ammonia, and soluble proteins.
Rectoromanoscopy: multiple erosions and ulcers, the mucous membrane is swollen,
hyperemic, bleeds even with light contact with the instrument, pseudopolyps, mucus in the
navel of the intestine, pus. Irrigoscopy: disappearance of gaustration, ulcerative
discolorations of various shapes, central and marginal filling defects caused by
pseudopolypes.
Treatment. The diet limits the amount of fat (in severe cases-up to 55-60 g) and
carbohydrates (200-250 g), the proportion of vegetable fiber is reduced as much as
possible; the diet should correspond to diet 4. If certain foods are intolerant, they are
excluded from the diet. Basic therapy: sulfasalazopreparations and glucocorticosteroids. In
mild forms, sulfasalazine is prescribed 3-4 g/day, in severe forms-8-12 g/day. For patients
with distal forms, rectal administration of sulfasalazine in suspensions of 4-6 g of the drug
in 50 ml of isotonic sodium chloride solution or in suppositories (1.5 g of sulfasalazine
and 1.5 g of cocoa butter) is recommended. In case of left-sided and total lesion, the
combined use of the drug (orally and topically) is appropriate. Salazodimethoxine and
salazopyridazine are long-acting drugs, the maximum dose of these drugs is 2 g / day (0.5
g 4 times a day). Sulfasalazine blocks folic acid transport, inhibits the activity of
enzymatic processes associated with folacin, so patients should be prescribed folic acid at
a dose of 0.002 g 3 times a day. The course of treatment with sulfasalazine is from 3-4 to
6-8 weeks or more in the therapeutic dose and then, reducing the dose by 0.5 every 10-14
days, maintenance therapy (0.5 g / day) - up to 6-12 months. Treatment with sulfasalazine
in 10-30% of cases is accompanied by the development of side effects, if they occur, the
drug should be discontinued until the complications are completely stopped. You can
resume taking the drug in half the dose, gradually increasing it to the therapeutic one. But
more often salofalk is prescribed: 1.5 g (6 tablets) daily for mild forms and 3 g/day - for
moderate forms. In severe cases, oral administration of salofalk is combined with enema
administration (4 g in 60 ml of isotonic sodium chloride solution) daily, once
after stools for 8-10 weeks, or using a suppository (0.5 g 3 times a day). Indications for the
use of glucocorticosteroids: 1) left-sided and total forms of ulcerative colitis with severe
course, III degree of activity; 2) acute severe and moderate forms of the disease with the
presence of extra-intestinal manifestations; 3) lack of effect from other methods of
treatment. The dose of prednisone is 0.5-1 mg / kg, and in acute severe forms 1-1. 5 mg /
kg per day inside or in candles (1 candle with 5 mg of prednisone). The indicated dose is
recommended to be taken until the therapeutic effect is achieved (3-4 weeks, less often up
to 6 weeks), then it is reduced by 10 mg every 10 days to 30 mg / day, and subsequently
the dose of prednisone is gradually reduced by 2.5mg every 7-10 days. The patient may
take a maintenance dose of 5 mg daily or, more appropriately, 10mg daily. The general
course of treatment with prednisone is 6-9 months. You can also use hydrocortisone at a
dose of 250-500 mg/day intramuscularly or 125 mg rectally. Patients take sulfasalazine or
salofalk until the hormones are completely removed. If you are refractory to basic drugs,
azathioprine is prescribed at a dose of 150 mg / day. Timely prevention of intestinal
dysbiosis is necessary (see Intestinal dysbiosis), broad-spectrum antibiotics are
recommended only if there is a threat of developing toxic megacolon, secondary purulent
infection. To normalize microcirculation, the treatment complex should include trental,
prodectin, parmidine, if indicated-calcium preparations, antihistamines. Timely correction
of protein metabolism (intravenous administration of 10-20% albumin solution, frozen
plasma is indicated), water - electrolyte balance disorders, and anemia is important. With
severe diarrhea, it is advisable to prescribe white clay (4-12 g / day), loperamide (2
capsules in the morning and 1 capsule after stool, but no more than 6 capsules per day). To
normalize digestion, pancreatin, mezim-forte, panzinorm are recommended (at least 2
tablets per meal, up to 4-6 weeks). It is necessary to prescribe B vitamins (B1, B6, B12),
ascorbic acid parenterally, inside vitamins A, E, lipoic acid are indicated.

3.3.4. Crohn's disease (terminal, regional ileitis, granulomatous enterocolitis) is a

chronic non-specific segmental or polysegmental transmural granulomatous inflammation
of the gastrointestinal tract. More often, the terminal ileum is affected, butany part of the
gastrointestinal tract can be involved in the pathological process - – from the oral cavity to
the anal region.
The etiology of the disease has not been established. The morphological substrate of
Crohn's disease is granuloma with epithelioid cells and giant and Langhans cells, localized
in the submucosal layer, in combination with hyperplasia of lymphoid follicles and
peripheral plaques. Infiltration by lymphocytes and plasma cells extends to the muscle and
subserous layers, which leads to narrowing of the intestinal lumen. The mucous membrane
remains intact for quite a long time, it rises above granulomatous infiltrates in the form of
bumps (a symptom of "cobblestone urinary tract"). Crevices are also formed-linear ulcers
that penetrate the submucosal layer, and often in the muscle forming fistulas, abscesses,
strictures. The process is segmental in nature, the length of damage is from 3-4 cm to 1 m
or more. There is a distinction between acute and chronic forms of Crohn's disease. The
acute form looks like acute appendicitis, since the process in most cases is localized in the
terminal ileum. Pain in the lower right quadrant of the abdomen rapidly increases, nausea,
vomiting appear, body temperature rises, accompanied by chills. As a rule, there is
growing flatulence, diarrhea with slime, sometimes with an admixture of blood. On
palpation of the abdomen, there are no signs of peritoneal irritation, although an infiltrate
in the right iliac region can be palpated. In the case of small bowel localization of the
chronic form of the disease, its main manifestations are meteorism, subfebrile body
temperature, mild abdominal pain that is not related to the nature and volume of food
taken, rumbling, abdominal transfusion, diarrhea (stool – 3-6 times a day, with mucus),
rectal bleeding of various intensity is possible. Gradually, the appetite decreases, weakness
joins, уменьшается масса body weight decreases, and malabsorption syndrome increases.
With colonic localization, process a includes abdominal pain of an indeterminate nature,
diarrhea, fever, and weight loss. The stool is semi-formed, 4-6 times a day, sometimes
watery. Extra-intestinal manifestations: aphthous stomatitis, erythema nodosum,
hyperkeratosis, опоясывающий shingles, psoriasis, furunculosis, uveitis, iridocyclitis,
uroarthritis, vascular lesions. Complications: perforation of ulcers with the formation of
limited infiltrates and abscesses, fistulas (rectovaginal, intestinal-cystic, colonic - small
intestinal), intestinal bleeding. Peritonitis, as a rule, is not observed. развиваться Intestinal
stenosis may develop кишки with a clinical picture of intestinal obstruction.
Diagnostics: peripheral blood examination (hyperchromicanemia, лейкоцитоз
поleukocytosis, increased ESR), coprological examination (leukocytes, red blood cells,
increased alkaline phosphatase content), bacteriological examinationof feces, biochemical
examination of plasma (hypoproteinemia, hypoalbuminemia, hypocholesterolemia,
decreased potassium, sodium, chlorides, calcium, iron). Irigoscopy: uneven narrowing of
the intestinal lumen, changes in the affected areas by the type of rigid tube, fistulas.
Colonoscopy: uneven thickening of the mucous membrane like a "cobblestone pavement",
edema, longitudinal and transverse deep cracks-ulcers. The biopsy is not very informative,
since the granuloma is located in the submucosal layer.
Treatment. Mechanically and chemically sparing diet with a sufficient content of
protein, vitamins and minerals, restriction or exclusion of milk when it is not consumed
and restriction of coarse vegetable fiber (diet No. 4). Basic therapy – sulfasalazine at a
dose of 3-6 g / day or mesalazine, 3 g/day. Salazopyridazine is used 2 g / day for 4 weeks,
and then 1.5 g / day for the next 3-4 weeks, the dose is reduced by 0.5 g every 10 days, the
patient takes a maintenance dose of 0.5 g/day for 4-6 weeks. Glucocorticosteroids are
indicated for frequent relapses of the disease, anemia, and systemic manifestations. The
initial dose of prednisone is 30-40mg/day, with a decrease in the activity of the process
(after 1-1.5 months), the dose of the drug is gradually reduced by 2.5 mg per week. The
duration of treatment with glucocorticosteroidsis 4-6 months. If glucocorticosteroids are
ineffective, azathioprine (1.52 mg/kg) or imuran (50 mg/day) are prescribed, which
reduces the dose of prednisone administered simultaneously to 20-30 mg/day. If fistulas
develop in the perineal region, trichopol 20 mg/kg is required, and if the disease activity
decreases, the dose of trichopol is reduced by 2 times. Broad -spectrum antibiotics
(cephalosporins, synthetic penicillins) are indicated for the treatment of opioid infection. If
necessary, protein preparations (plasma, albumin), glucose-saltыsolutions, B vitamins,
ascorbic acid, folic acid, vitamin D, A, E. According to indications, adsorbent-enveloping,
enzymatic preparations are used. The intestinal microbial spectrum is corrected, and drugs
that improve microcirculation, trophism, and mucosal repair (curantil, riboxin, eufillin, and
methyluracil) are prescribed. Indications for surgical treatment are: intestinal stenosis,
fistulas, perforation стенки of the intestinal wall, septic complications, failure of long
-term conservative treatment.

3.3.5. Ischemic colitis. The term combines various clinical forms of vascular lesions of
the colon. In the course of ischemic colon disease can be acute and chronic. Acute
ischemia of the colon develops due to acute occlusive lesion of the suckers (thrombosis,
embolism) or a rapidly occurring hypovolemic state (shock, collapse). Intestinal lesions
maybe reversible, but gangrene develops more frequently. Restriction of blood flow due to
atherosclerosis of the abdominal cavity, heart failure, and vasculitis leads to a chronic form
of ischemic bowel disease (ischemic colitis with stricture formation). Acute forms are
more often characterized by damage to the entire intestine, while chronic forms are
characterized by segmental lesions, usually in thereof the night bend and the upper part of
the sigmoid colon. With intestinal gangrene, a picture of an acute abdomen develops.
Transient ischemia is manifested by pain, repeated intestinal bleeding, and unstable stools
with pathological admixtures. The degree of severity of certain symptoms is determined
by the form of ischemic colon disease. The reversible form is characterized by acutely
occurring severe abdominal pain, which can also quickly disappear spontaneously. Pain is
more often localized in the left abdomen, combined with tenesmus, and in the next day
they are joined by intestinal bleeding. Approximately half of the patients experience
vomiting and diarrhea. In severe cases, fever, tachycardia, leukocytosis are noted, which
serve as signs of progression of the process. Palpation of the abdomen reveals soreness
along the colon, sometimes symptoms of irritation of the peritoneum. There are two
possible outcomes of the reversible form of ischemic colon disease — resolution of the
process or transition to an irreversible form. The irreversible form is manifested by the
formation of a stricture of the colon or the development of its gangrene. The clinical
picture of irreversible ischemic colon disease with stricture formation is dominated by the
symptoms of intestinal obstruction. In the gangrenous form of the disease, in addition to
acute болей abdominal pain and shock, bleeding and diarrhea due to necrosis of the
intestinal wall often come to the fore. These symptoms are combined with manifestations
of peritonitis.
Diagnostics. The clinical picture only allows us to suspect intestinal ischemia. During
colonoscopy, erosive and ulcerative changes are detected in the form of defects in the
mucous membrane of an irregular shape. During irrigoscopy, intestinal spasm, loss of
gaustration, contour unevenness, or tubular narrowing are detected in the altered segment.
Selective angiography reveals direct signs of occlusive lesions.
Treatment. Treatment of reversible intestinal ischemia consists in prescribing a gentle
diet, light laxatives, vasodilators and antiplatelet agents. In the case of a secondary
infection, antibiotics or sulfonamide preparations are prescribed. If the disease is more
severe (signs of intestinal obstruction, gangrenous form), surgical treatment is indicated.

3.3.6. Eosinophilic gastroenteritis is an allergic disease characterized by eosinophilic

infiltration of the mucosa and muscle layer of the stomach and small intestine.
The clinical picture is dominated by chronic diarrhea, leading to a decline in nutrition.
Diagnosis is based on the combination of the clinic with food, respiratory and skin allergic
reactions, blood eosinophilia, eosinophilic infiltration of biopsy samples of the gastric
mucosa and duodenum 12, and an increase in the level of immunoglobulin E in the blood.
In the treatment of corticosteroids, the main place is occupied by corticosteroids.
3.3.7. Diverticular disease of the colon is a disease characterized by the formation of
blind sac – like protrusions-diverticulae. False diverticula usually form in the colon,
because only the mucous membrane protrudes through weak areas of the muscle layer
along the vessels. Diverticular disease develops mainly in the elderly and affects mainly
the sigmoid colon, less often the right half поперечной of the transverse colon, and very
rarely the rectum.
Clinical picture. The disease can be asymptomatic for a long time or manifest it self in
constipation and moderate bloating of the intestine. Some patients have sharp spastic
abdominal pain. Inflammation of the diverticula (diverticulitis, per diverticulitis, abscess)
is accompanied by pain, fever, tension of the abdominal wall, more often in the lower left
quadrant of the abdomen, signs of obstruction and neutrophilic leukocytosis. When the
diverticulum is perforated, peritonitis develops.
Diagnostics. The diagnosis is established on the basis of the results of X-ray and
endoscopic examination.
Treatment. A diet containing a large amount of vegetable fiber; wheat bran, the amount
of which in the diet is increased gradually over 2-4 weeks (from 5-10 to 20 g per day);
means that normalize the motor activity of the colon. Regulatory effects can be provided
by prokinetics (domperidone, coordinax). In case of diverticulitis , the intestine is sanitized
with the help of antibacterial drugs: broad-spectrum antibiotics, hard-to-dissolve
sulfonamide preparations (phthalazole, sulgin, sulfasalazine), intetrix, enterol. Surgical
treatment is indicated for complicated diverticulitis (perforation, abscess, obstruction).

3.3.8. Intestinal dysbiosis. The microflora of the colon of a healthy person consists of
90% anaerobes (bifidobacteria and bacteroids).Aerobes (Escherichia coli, Streptococcus,
lactobacilli, enterococci) account for only 10%. The contents of the small intestine are
sterile or contain a small number of microbes. Changes in the quantitative and qualitative
composition of normal microflora are referred to as "dysbacteriosis" or "dysbiosis".
Dysbiosis of the first degree significantly reduces the number of normal symbiotes in
their natural habitats.
Grade II dysbacteriosis is characterized by the disappearance of some symbionts and an
increase in others, sometimes with changes in their properties (hemolytic, lactose-negative
or weakly enzymatic escherichia coli), as well as the proliferation of bacterial flora in the
small intestine.
In dysbiosis of the third degree, pathogenic strains of bacteria (proteus, staphylococci,
Clostridium), as well as fungi, appear against the background of a pronounced violation of
the normal ratio of microbiocenosis).
The cause of dysbiosis is often the irrational use of antibacterial drugs, which leads to
the death of a significant part of the normal microflora that is sensitive to the drug, and
rapid reproduction of microorganisms resident to it. The development of dysbiosis is
promoted by poor nutrition, prolonged retention of feces in the colon, as well as diseases
that occur with intestinal damage. Changes in the bacterial flora and its proliferation in the
small intestine are caused by a violation of general and local immunity, a decrease in the
production of lysozyme in the mucous membrane, and a lack of enzymatic digestive
systems. In dysbiosis, the main properties of the normal microflora of the colon are
disrupted – it sanaphonic activity against pathogenic microorganisms,
vitamin-synthesizing, enzymatic and immunological functions.
Clinical picture. Dysbiosis may протекать be asymptomatic or manifest as
gastrointestinal dysfunction (abdominal pain, flatulence, stool disorders). The general
condition of the patient usually does not change.
Diagnostics. The diagnosis is established on the basis of the clinical picture, taking into
account the anamnesis, concomitant diseases and the results of bacteriological
examination of the CAla. For the diagnosis of hyper proliferation of bacterial flora in the
small intestine, seeding and gas-liquid chromatography of jejunum soda with the
determination of volatile fatty acids, as well as a respiratory hydrogen test, are performed.
Treatment. Both antibacterial drugs and products containing normal intestinal flora are
used. Antibacterial drugs are prescribed during the period of exacerbation in order to
suppress the growth of pathogenic microbes. Intestinal antiseptics (enteroseptol, intetrix,
enterol), sulfonamide preparations (phthalazole, sulfasalazine) are indicated for 10-14 days
in patients with dysbiosis of the first and second degrees. In staphylococcal dysbiosis,
erythromycin or oxacillin are prescribed, as well as staphylococcal gamma globulin,
toxoid and bacteriophage. Nitrofuran preparations (furazolidone, furadonin) or
nevigramon (negram) are used to eliminate proteinaceous dysbiosis. In cases of
association of microbes with fungi, nystatin or levorin is prescribed simultaneously. The
duration of the course of anti-bacterial therapy is 7-14 days. After its completion cultures
of bacterial preparations (colibacterin, bifidumbacterin, bificol, bactisubtil, linex) are used
to achieve a more stable reaction. They cause a temporary increase in the number of
normal bacteria in the colon.

3.3.9. Intestinal tuberculosis is rare and belongs to the group of tuberculosis of other
organs and systems (extrapulmonary). Intestinal tuberculosis can be primary or secondary.
Primary tuberculosis most often has an alimentary origin, its development is associated
with Mycobacterium bovine species (Mycobacterium bowis), which enters the intestines
with milk and dairy products. Secondary intestinal tuberculosis is more often diagnosed as
a result of intra-intestinal infection by sputum ingestion in patients with pulmonary
tuberculosis, mycobacteria can enter the intestine by hematogenic or lymphogenic route in
patients with extrapulmonary tuberculosis (Mycobacterium tuberculosis or africanum).
Tuberculosis is characterized by segmental intestinal damage overa small area. The most
typical localization is the terminal ileum and cecum-tuberculousileotiflitis .
Clinical picture. In the initial period, intestinal tuberculosis may be asymptomatic: loss
of appetite, nausea, heaviness in the abdomen after eating weakness, subfebrile body
temperature, sweating at night, weight loss, unstable stools, flatulence. Subsequently, there
is constant pain in the right half of the abdomen, in the right iliac region, near the navel,
which does not depend on food intake, its quality and quantity, constant flatulence with
abundant gas discharge, liquid stool, frequent with an admixture of blood and mucus.
Palpation of the abdomen may reveal a painful thickened cecum, and sometimes a
tumor-like formation (enlarged lymph nodes) is palpated in the right iliac region. With the
development of tuberculous mesadenitis – pain to the left of the navel and inside of the
cecum along the mesentery of the small intestine, enlarged lymph nodes can be palpated.
The diagnosis is supported by data on contact with the patient and tuberculosis, the
presence of tuberculosis of a different localization, and detention in places of deprivation
of liberty. Hemogram: hypochromic anemia, leukopenia with relative lymphocytosis, ESR
increase. In the coprogram, tuberculosis mycobacteria are detected very rarely. Tubercaine
samples are usually positive. Irrigoscopy and survey radiography of the abdominal cavity:
wall rigidity, filling defects and stenoses in the ileocecal region, abdominal adhesions
calcification of mesenteric lymph nodes. Colonoscopy: edema, hyperemia of the mucous
membrane, the presence of ulcers with hidden edges, rigidity of the intestinal narrowing
wall, specific (tubercular) rashes on the mucosa may be detected. A biopsy: epithelioid
granulomas with giant Pirogov-Langhansa cells and caseosis. Ultrasound examination
reveals the so-called "hollow organ lesion symptom" – an ultrasound image of an oval
shape with an anechoic periphery and an echogenic center.
The progression of the inflammatory process and infiltration in the affected area is replaced by
fibrosis, wrinkling and scarring, which can lead to стенозу intestinal stenosis.
Treatment is carried out in a specialized tuberculosis hospital.

3.3.10. Whipple's disease (intestinal lipodystrophy, granulomatous lipodystrophy,

mesenteric hiladenectasia) is a rare systemic disease with predominant small bowel
damage, occurring with arthralgia, diarrhea, and exhaustion. In 80% of cases, men aged
40-49 are ill. The etiology of the disease and Whipple remains unclear. Most likely, this is
an infectious disease, which is supported by the detection of small gram-positive
microorganisms in the active phase in the mucosa of the small intestine and in other organs
involved in the pathological process, called Whipple bacilli. The disease is based on
infiltration of the mucosal lamina proper, blockade of the lymphatic vessels of the small
intestine, mesentery and mesentery lymph nodes by PAS-positive macrophages, which
makes it difficult to transport nutrients to the blood and lymphatic vessels.
Clinical picture. At the initial stage, extra-intestinal manifestations predominate:
migrating polyarthritis (polyarthralgia), bronchitis, subfebrilebody temperature,
indeterminate abdominal pain, and fatigue. Later (at the first stage), metorism, diarrhea
(copious, light, sometimes chylous stools up to 10 times a day), rarely constipation, weight
loss, and lymphadenopathy are added. There is a brown pigmentation of the oral mucosa,
aphthae, smoothness of the papillae of the tongue, hemorrhages and nasal erythema appear
on the skin. Anemia, achlorhydria, hypoproteinemia, hypocalcemia, hypoпо-vitamin
deficiency, fever are noted. The third stage is characterized by the development of
cachexia, the appearance and progression of systemic lesions: pancarditis, polyserositis,
hepatosplenomegaly. Neurological symptoms increase, 6-10% of patients develop
oculomotor paresis, hearing and vision disorders, ataxia, nystagmus, tremor, signs of
dementia appear, возможны polydipsia and polyphagia are possible.
Diagnosis is extremely difficult. Patients have significantly increased ESR, reduced
hemoglobin level, increased the number of white blood cells and platelets. The
concentration of protein, iron, calcium, and cholesterol in the blood serum decreases.
Steatorrhea is typical (fat loss reaches 50 g per day and above). Endoscopy of the
duodenum sacrum with biopsy, assimilation biopsy of the small intestine are important.
Duodenoscopy: the intestinal mucosa is swollen, hyperemic, and its relief is uneven due to
numerous, slightly elevated formations of light yellow color. Histological and especially
ultrastructural examination of biopsies reveals a pronounced infiltration of the own
mucosal layer оболочки by PAS-positive macrophages.
Treatment. Diet: replacing normal fats with medium-and short-chain fats (fat products
such as portalac) leads to a rapid reduction in steatorrhea and malabsorption syndrome.
Antibiotics (tetracycline, doxycycline, clindamycin, and others) are used in maximum
pharmacopoeial doses for a long time-from 6 months to a year or more. In cases of
tetracycline intolerance, penicillin is used in combination with streptomycin (the doseиof
penicillin is 1200,000 U/day, streptomycin - 1 g / day) в for 10-14 days intramuscularly,
and then antibiotics are administered orally for up to 2-5 months. Correction of anemia,
vitamin deficiency, mineral and protein metabolism is performed. Enzyme antidiarrheal
and adsorbent drugs are prescribed.

3.4.1. A carcinoid is a potentially malignant tumor that originates from the chromaffin
cells of the deep parts of the intestinal crypts (Lieberkunian glands). In 46-75% of cases,
the carcinoid is localized in the appendix, in 20-28% - in the saliva and ileum,
significantly less often there are tumors of other localization (in the rectum, stomach,
pancreas). A carcinoid can develop multicentrically from endocrine cells scattered in the
gastrointestinal tract. The incidence of malignancy and metastasis of the carcinoid varies
from 5 to 55%.
Clinical picture. There are local signs of a tumor and a carcinoid syndrome caused by
the action of biologically active substances and hormones (serotonin, bradykinin,
histamine, prostaglandins). Carcinoid syndrome is characterized by the following signs:
• attacks of redness of the upper half of the body with a feeling of heat, accompanied
повышеннымby increased sweating and palpitation;
• diarrhea with cramping болями в abdominal pain;
• attacks of suffocation due to bronchospasm.
Prolonged intake в кровь of active vasodilating compounds in the blood leads to the
development of persistent cyanosis, telangiectasia, dermatosis, arthralgia, right ventricular
heart failure due to the development of fibrosis of the right heart. Carcinoid syndrome
develops only in 8-10% of patients, usually with metastasis of the tumor to the liver.
Diagnostics. The diagnosis is established on the basis of clinical and radiological
data. Contrast X-ray examination: possible filling defects or niche symptom in case of
ulceration of the tumor. Determination of serotonin in the blood and its metabolite
(5-hydroxyindoleacetic acid) in the urine.
Treatment of malignant carcinoidis surgical-radical removal of the tumor and its
metastases. If it is impossible to perform cancer surgery, symptomatic treatment is
recommended: adrenoblockers (phentolamine, anapriline), serotonin antagonists (deseryl,
peritol), kinin inhibitors ( kontrikal, trasilol), antihistamines, sandostatin (octreotide) at a
dose of 0.05-0.2 mg 2-3 times a day intramuscularly.

3.4.2. Small bowel lymphoma is a malignant tumor of the lymphoid tissue. Primary
lymphoma can be focal and diffuse with total damage to the small intestine. Diffuse
lymphoma of the small intestine is distinguished as a special form and is usually referred
to as "Mediterranean-type lymphoma", since itis distributed mainly in the Mid-European
region. Often, this type of lymphoma is combined with a disease of heavy α- chains,
which is explained by a violation of the synthesis of immunoglobulins in these diseases.
Clinical picture. Diarrhea is the leading symptom, stool frequency is 3-4 times a day,
and fecal matter is usually plentiful. In severe cases, the frequency of stool reaches 10
times a day. There are abdominal pains of varying intensity and localization, nausea,
vomiting, anorexia, weakness, rapid fatigue, significant weight loss and dehydration,
edema and ascites may appear. On examination: the patient is emaciated, the abdomen is
enlarged, sometimes it is possible to detect a tumor formation.
Diagnosis is based on the clinical picture, hemogram (moderate anemia and increased
ESR, hypoproteinemia and hypoalbuminemia), X-ray picture (diffuse thickening of folds
along the entire small intestine), mucosal biopsy data (massive infiltrates from
mononuclears). Thick folds of the duodenal mucosa can also be detected и endoscopically.
Treatment. Cytostatic chemotherapy is ineffective in patients with diffuse small bowel
lymphoma. The best results are achieved when taking tetracycline in a severe dose of 1-2
g. Symptomatic treatment is aimed at normalizing water-salt and protein metabolism.

3.5.1. Lactase deficiency (lactose malabsorption) is the most common form of

disaccharide- deficiency enteropathy, which is manifested by milk intolerance syndrome.
Lactase is an enzyme in the small intestine that breaks down milk sugar (lactose) into
glucose and galactose.
To date, three forms of lactase deficiency have been identified.
Hereditary congenital lactase deficiency (congenital alactasia) in infants. It is rare,
characterized by profuse water diarrhea that occurs after the first feeding of the child, rapidly
increasing hypotrophy and dystrophy, if the child continues to be fed milk, including maternal
milk.

Congenital lactase insufficiency in adults (type with delayed onset) is characterized by

good milk tolerance during breastfeeding, and at the age of 2-4 years and older , hypo - or
alactasia with a clinical picture of lactose malabsorption develops due to regression of the
gene encoding lactase synthesis.
Secondary lactase deficiency is associated with changes in the epithelium of the small
intestine under the influence of diffuse mucosal lesions in diseases and toxic effects. As a
result, the activity of all disaccharidases and other enzymes decreases, but the activity of
lactase decreases most significantly.
Clinical picture. Usually, 30 minutes – 2 hours after taking milk and other dairy
products, the patient develops bloating, transfusion, rumbling in the abdomen, cutting
(spastic) pain along the bowel, often accompanied by the discharge of a large amount of
gases and liquid stools with the release of foamy watery feces of light yellow color with a
sour smell. There may also be a gruel-shaped stool, a polyfectomy. Lactose malabsorption
is accompanied by a deficiency of minerals, vitamins, and sometimes protein,
osteoporosis, and can lead to the development of dysbiosis and dystrophic changes in the
intestinal mucosa. Toverify the diagnosis of lactase deficiency, we use the assessment of
clinical manifestations after a lactose or milk load with a parallel study of feces (pH,
уровень lactose level); tests на for lactose tolerance, hydrogen test: determination of the
level of hydrogen in the exhaled air after a lactose load. A hydrogen level above 20 pg / ml
is considered a reliable criterion for lactic-pelvic insufficiency. The diagnosis is also
confirmed by the disappearance of symptoms of the disease after the exclusion из пищи of
milk and dairy products from food.
Treatment of lactase deficiency consists in excluding milk and other dairy products
(except fermented cheeses), orusing it in small quantities (no more than 1 cup during the
day), or using milk in the form of cereals, puddings. Lactose-free dairy products are used
in the diet: "Alactosit N", lactose-free enpit, вместо молока yogurt is used instead of milk
.

3.5.2. Gluten enteropathy (celiac disease, celiac disease, non-tropical enteropathy) is a

disease characterized by a lack of enzymes that break down the protein of cereals-gluten
and its fractions (gliadin), with secondary toxic and immune damage to the mucosa of the
small intestine. Gluten enteropathy can be congenital or (less often) acquired. The cause of
gluten enteropathy is the congenital absence or acquired insufficiency of gliadinamidase,
an enzyme produced by enterocytes that breaks down the gliadin of the gluten protein of
cereals (rye, wheat, barley, oats). Gliadin accumulates in the small intestinal cavity and
exerts a cytotoxic effect on epithelial and crypt cells. Secondary gluten enteropathy is also
observed with prolonged antimiotictherapy, fasting, chronic mercury poisoning, and
diseases associated with increased intestinal wall permeability .
Clinical picture. The first manifestations are more often observed in infancy, as soon as
gluten-containing products are included in the diet (milkmixtures, cereals, biscuits, bread,
crackers). There are repeated, often persistent diarrhea, hypotrophy, and developmental
delay. If adequate treatment is not prescribed, cereal intolerance may last throughout
childhood, but decreases in adolescence or disappears completely, resuming at the age of
30 to 40 years. During the exacerbation, bloating, rumbling, and transfusion are
characteristic. Stool up to 10-15 times a day, watery or gray, greasy, foamy, less often
semi-formed, gray-brown in color, has a fetid rancid smell, floats in water. Body weight
loss, weakness, rapid fatigue, adrenal cortical insufficiency, hypokalemia, multifactorial
anemia, gastrointestinal, uterine, nosebleeds (vitamin C and K deficiency), osteomyelitis
and osteoporosis, spontaneous bone fractures ( vitamin D, calcium, phosphorus
deficiency), muscle weakness, and paresthesia with loss of weight are noted sensitivity,
ataxia, peripheral poly-neuropathies, signs of encephalopathy (B vitamin deficiency ).
Objectively: weight loss, muscle atrophy, hypotension, symptoms of "tympanic
patches", "frequent glasses", dry skin, hypoproteinemic edema, especially on the
extremities, glossitis, cheilitis. The abdomen is swollen and enlarged. Hepatomegaly is
detected in severe cases, ascites is possible.
In the blood test: micro-and macrocytic anemia, leukopenia, thrombocytopenia,
increased ESR. Iron levels are low, prothrombin time is prolonged, the content of sodium,
potassium, chlorides, calcium, phosphorus, and zinc decreases, hypoproteinemia with
hypoalbuminemia and hypergamaglobulinemia is detected, and cholesterol levels
decrease. Ina colological study, most patients have steatorrhea, creatorrhea due to muscle
fibers without striation; in a bacteriological study of feces, associated dysbiosis with a
predominant growth of proteus, hemolytic forms of Escherichia coli, yeast – like fungi is
observed. The D-xylose test confirms malabsorption in the small intestine. A biopsy of the
small intestine mucosa reveals an increase in the number of goblet cells, subtotal or total
villi atrophy, and an increase in the number of interepithelial and plasma cells.
The diagnosis of gluten enteropathy is confirmed by the detection of gliadin in plasma
and urine, as well as the presence of antibodies to gliadin and gluten, a decrease in
the level of gliadinamidase in intestinal juice and in a biopsy of the small intestine
mucosa, and the effectiveness of a gluten -free diet.
Treatment. The basis of treatment of patients with gluten enteropathy is a diet with the
complete exclusion of gluten from wheat, rye, barley, and oats – No. 4a. Rice, soybeans,
corn, rice flour, millet, potatoes, vegetables, fruits, berries, animal products are completely
non-toxic, and they should be widely used in the diet of patients. It is only necessary to
limit dairy products, as often gluten enteropathy develops hypolactasia.
In case of a severe course of the disease, glucocorticosteroids are prescribed (20-40 mg
of prednisone), the course of treatment is 3-6 months. Special attention is paid to the
normalization of protein metabolism, water-electrolyte and vitamin balance, correction of
anemia and digestive disorders. Symptomatic therapy includes adsorbents, astringents,
enveloping agents that normalize trophism and microcirculation.

3.6.1. Dumping syndrome is the most common disorder after gastric resection. The
syndrome mainly develops у in patients who have undergone Billroth surgery II. The
dumping syndrome is based on rapid evacuation of food from the stump of the stomach
due to the loss of its reservoir function and accelerated passage of food masses through the
small intestine. The penetration of coarse, hyperosmolar food into the small intestine leads
to a number of disorders:
• an increase in osmotic pressure in the intestine with the diffusion of fluid into its
lumen and, as a result, a decrease in the volume of circulating blood;
• rapid absorption of carbohydrates that stimulate the excess release of insulin,
withной a change from hyperglycemia to hypoglycemia;
• irritation of the receptor apparatus of the small intestine, which leads to stimulation
of the release of biologically active substances (acetylcholine, kinins, histamine,
catecholaminob) and an increase in the level of gastrointestinal hormones.
The clinical picture is represented by a combination of vasomotor disorders
(weakness, sweating, palpitation, dizziness, sometimes fainting, feeling hot, pallor or
flushing of the face, changes in pulse and blood pressure), and gastrointestinal disorders
(heaviness and discomfort in the epigastric region, nausea, vomiting, belching, flatulence,
diarrhea). These phenomena occur during meals or after 10-20 minutes after taking food,
especially sweet and dairy dishes. The duration of attacks is from 10 minutes to several
hours. The diagnosis is based on the characteristic clinical picture. For X-ray examination
the study shows rapid evacuation of barium suspension ("discharge") from the stump of
the stomach and accelerated passage through тонкой the small intestine.
Treatment. Diet: the food should be varied, high-calorie, with a high content of
protein, vitamins, normal fat and complex carbohydrates with a sharp restriction of simple
carbohydrates. Прием Food intake should be fractional, не at least 6 times a day. It is
recommended to start a meal with dense dishes, after eating, it is advisable to lie in bed or
recline in a chair for 20-30 minutes. Pharmacotherapy: local anesthetics (0.5% novocaine
solution of 30-50 ml, almagel A, 0.3 g anesthesin orally 20-30 minutes before meals),
anticholinergic and ganglion blocking agents (gastrotsepin-50 mg, no-shpa-0.04 g,
benzohexonium 0.1 g 2-3 times a day), tranquilizing and sedative agents drugs (elenium,
tazepam по 0.01 g 2-3 times a day, seduxen по 0.005 g 1-2 times a day), multi-enzyme
preparations (mezim-forte, panzinorm, etc.). In the absence of the effectiveness of
conservative therapy, reconstructive surgery is performed.

3.7.1. Zollinger-Ellison syndrome is a gastrin-producing tumor that in 85-90% of cases

is localized in the pancreas, while in the remaining 10-15% of cases it may be located in
other organs (most often in the duodenum). It is characterized by multiple, usually
recurrent postbulbar duodenal ulcers that are resistant to therapy. Often these are peptic
ulcers of the stomach stump after resection for peptic ulcerной disease. It is characterized
by a high level of basal acid production, an increase in the level of gastrin in the blood
serum (up to 1000 ng / ml), diarrhea, and repeated bleeding. At lower rates of gastrinemia,
a cretin test is performed. The test is considered positive if the level of gastrin in the blood
serum increases by more than 200 ng / ml after intramuscular administration of 2 ME
secretin. The tumor is diagnosed using ultrasound methods. Radical treatment involves
detection and removal of the tumor. Conservative therapy consists of long-term
administration of high doses of antisecretory drugs, for example, ranitidine up to 6 g / day
or omeprazole.
Separately, we should focus on functional muscle disorders, when diarrhea,
constipation or their alternation are not explained in the results of laboratory, instrumental
and morphological studies.

3.8. Irritable bowel syndrome (IBS) is a biopsychosocial functional disorder of the

bowel, which is based on the interaction of two main mechanisms: psychosocial influence
and sensorimotor dysfunction, i.e. disorders of visceral sensitivity and motor activity.
Characterization of the syndrome requires a special strategy for diagnosis, differential
diagnosis, and implementation of a treatment program.
The prevalence of IBS in most countries of the world is high and amounts to 15-20%,
despite the fact that 2/3 of people experiencing symptoms of IBS do not go to doctors. The
peak incidence occurs in the young working age-30-4 0 years. The ratio of women to men
ranges from 1: 1 to 2:1.
In 1988, in Rome, the International Group for the Study of Functional Pathology of the
Gastrointestinal Tract (GIT) for the first time officially defined the term "fractured bowel
syndrome", defined it and developed a methodology for diagnosis, which later became
known as the "Rome Criteria for IBS".
In 1999, the criteria were supplemented and the Rome IBS II Criteria were adopted.
According to the criteria, IBS is a stable set of functional disorders lasting at least 12
weeks. during the last 12 months, pain and/or abdominal discomfort that disappear after
defecation are accompanied by changes in the frequency and consistency of stool and are
combined for 25% of the time of the disease with at least two persistent symptoms of
intestinal dysfunction-changes in the frequency of stool, stool consistency, and the act of
defecation itself (imperative urge, tenesmus, feeling of incomplete bowel emptying, extra
effort during defecation), mucus discharge with feces, flatulence (Table 1).

Rome criteria for IBS

combined
with abdominal pain or Two or more of the following symptoms are associated
discomfort, that: with changes in stool consistency during 1/4 of this
• pass symptoms after the act of time:
defecation • changes in the frequency of stools (more than
• are associated with changes in 3 times a day or less than 3 times a week)
the frequency of stool (constipation, • changes in the shape of feces (liquid, solid)
diarrhea, or their alternation) • changes in the act of defecation
• related to change in stool • imperative urges
consistency • feeling of incomplete emptying
• additional pulling, effort
• mucus discharge mucus
• production flatulence/bloating
 F. Weber and R. McCllum proposed a clinical classification in which, depending
on the leading symptom , three variants of the course of IBS are distinguished:
with predominant abdominal pain and
flatulence; with predominant diarrhea;
with prevailing constipation.
Identifying IBS variants is important from a practical point of view, as it determines the
choice of treatment. However, this division is conditional, since half of the patients have a
high frequency of combining various symptoms and transforming one form of IBS into
another (for example, when constipation changes to diarrhea and vice versa), which makes
it difficult to determine the dominant manifestation of the disease.
Two types of visceral hypersensitivity were found in patients with IBS:
1) lower pain perception threshold and 2) more intense pain sensation at the normal
perception threshold. The condition for the formation of visceral hypersensitivity is the
impact of so-called sensitizing factors, including intestinal infection (in particular, past
dysentery), psychosocial stress, and physical trauma, which are somehow associated with
abdominal pain. Clinical manifestations of visceral hypersensitivity include hyperalgesia
and allodynia. Hyperalgesia can manifest itself as an increased sensitivity to pain stimuli
and a sensation of pain caused by non-painful stimuli. Allodynia is a functional disorder
caused by pain. Symptoms of IBS such as flatulence, impaired motility, transit, and
defecation are considered secondary to pain syndrome. In practice, allodynia is confirmed
by the observed transitions from one clinical form of IBS to another, as well as by the
results of treatment, when the pain syndrome subsides, a decrease in flatulence and
normalization of stool are noted.
In general, the development model of IBS can be presented as follows. In the presence
of a genetic predisposition and the influence of a sensitizing factor, a person developing in
a certain social environment develops a psychological type, in which, with a low level of
resistance to stress and weak social support, visceral sensitivity and intestinal motility are
disrupted, enterocerebral connections are broken, and a symptom complex of irritable
bowel is formed. It is very likely that IBS is neither a pathology of the gastrointestinal
tract, nor a disease of the central nervous system or the mental sphere. Most likely, this is a
new bio-neuropsychosocial state of a person, formed in extreme social conditions and
manifested by hyper-perception and hyper reactivity.
Diagnosis of the syndrome is based on the assessment of a persistent set of clinical
symptoms- lower abdominal pain combined with distal bowel flexion disorders, which are
not explained by currently known morphological and metabolic disorders, i.e. it is limited
to the exception of organic pathology.
Abdominal pain is a mandatory component of IBS. It can have a wide spectrum of
intensity: from mild discomfort, persistent aching pain to intense constant and even
unbearable, imitating the picture of intestinal colic. Patients with IBS are characterized
by pain immediately after eating, which is accompanied by bloating, increased peristalsis,
rumbling, diarrhea, or reduced stool. The pain subsides after defecation and discharge of
gases and, as a rule, does not bother at night. Pain syndrome in IBS is not accompanied by
weight loss, fever, anemia, or an increase in ESR.
Auxiliary symptoms that help determine the course of IBS include symptoms of
impaired transit and defecation. According to the Rome criteria, the frequency of stools
more than 3 times a day (diarrhea) and less than 3 times a week (binge drinking) is
considered pathologic. IBS is characterized by morning diarrhea that occurs after breakfast
and in the first half of the day, and the absence of diarrhea at night. About half of the
patients report an admixture of mucus in the feces, the composition and origin of which
are not determined. Excretion of blood and feces, nocturnal diarrhea, malabsorption
syndrome, and weight loss are considered «anxiety" symptoms that exclude the diagnosis
of IBS and require persistent search for an organic disease (Table 2).
 Patients are distinguished by an abundance of concomitant complaints and
personal characteristics that help to suspect IBS even at the first contact. Numerous
complaints can be divided into 3 groups:
symptoms of neurological and autonomic disorders-migraine, lumbar pain, lump in the
throat, drowsiness, insomnia, various types of dysuria, dysmenorrhea, impotention, etc .,
occurring у in 50% of patients;
symptoms of concomitant functional diseases of the digestive system - heaviness in the
epigastrium, nausea, belching, vomiting, pain in the right hypochondrium, etc., observed
in 80% of patients;
signs of psychopathological disorders, more often such as depression, anxiety
syndrome, phobias, hysteria, panic attacks, hypochondria , etc., are detected in 15-30% of
patients.

Symptoms of "anxiety" that exclude the diagnosis of

IBS
Complaints and anamnesis Physical examination
• unmotivated weight loss • fever
• nocturnal symptoms • changes in status (hepatomegaly,
• persistent intense abdominal pain as the splenomegaly, и etc.)
only and leading symptom of gastrointestinal Laboratory parameters:
tract damage • blood in the stool
• onset in old the elderly • leukocytosis
• colon cancer у in relatives • anemia
• increased ESR
• changes in blood chemistry
The non-specific nature of the clinical manifestations of intestinal damage makes it
extremely difficult to make a diagnosis at the nosological level. It is much easier to
determine which syndrome the symptoms fit into and start symptomatic treatment.
Choosing a more easy way of syndrome diagnosis is fraught with gross diagnostic errors
and an increased risk of late diagnosis of organic disease. In this regard, a specific strategy
for the diagnosis of IBS has been adopted.
The process of diagnosing IBS takes place in V stages.
At the first stage, the simplest causes of intestinal irritation are excluded, which include
chronic exposure to dietary factors and medications, and apreliminary diagnosis is made.
Common food irritants include fatty foods, alcoholic beverages, coffee, gas-forming
products and beverages, heavy (banished) food, and changes in dietary habits during
business trips and travel. Among the medicinal products that irritate the intestines are
laxatives, antibiotics, potassium, iron, bile acids, mesoprostol , etc.
On II - the dominant symptom and, accordingly, the clinical form of the syndrome are
distinguished.
At stage III - , the symptoms of "anxiety" are eliminated and a differential diagnosis is
made.
At stage IV, screening for organic disease is completed when performing the optimal
diagnostic tests, which includes clinical and biochemical blood tests, coprological
examination with stool analysis for worm eggs and giardia cysts, FEGDS, ultrasound of
the abdominal and pelvic organs, sigmo - or colonoscopy and irrigoscopy.
At stage V, a primary course of treatment is prescribed for at least 6 weeks, after which
the diagnosis is evaluated again. If the treatment is effective, a definitive diagnosis of IBS
can be made, and if it is ineffective, an additional examination is performed.
In the case of pain, diagnostic tests such as serial enterography, intestinal manometry,
balloon dilation test can be of the greatest value; in the case of diarrhea, the lactose
tolerance test, aspiration of the contents of the small intestine for the study of bacterial
flora; in constipation, the radioisotope transit study, the study of anorectal functions, etc.
The prognosis of the disease is favorable. The course of the disease is chronic,
recurrent, but not progressive. IBS has no complications. The risk of developing
inflammatory bowel diseases and colorectal cancer in patients with IBS is the same as in
the general population. This determines the tactics of monitoring patients and the absence
of the need for more frequent colonoscopies. The doctor should introduce patients to the
features of the disease prognosis, which will improve their psychosocial adaptation.
The treatment program consists of two stages-the primary course and subsequent basic
therapy. Implementation of the program requires a long time: the duration of the primary
course of treatment is at least 6 weeks, and the duration of basic therapy is 1-3 months.
The choice of program is determined by the interaction of several factors and depends on
the leading symptom (pain / flatulence, diarrhea, constipation), its severity and impact on
the quality of life, as well as on the patient's behavior and его mental state.
The main element of the program is the solution of the problem of psychosocial
adaptation with the obligatory involvement of the patient in the process of diagnosis and
treatment. Patients ' attention should be focused on the normal parameters of the study and
the importance of the absence of pathological disorders for the prognosis of the disease
should be emphasized. The patient must believe that he does not have a serious organic
disease that threatens his life. It is necessary to carefully ask the patient about the
conditions of nutrition, life, work, поtry to determine the sensitizing factor and the causes
of the disease. Next, the doctor should inform the patient about the nature of the disease
and tell them about the prognosis. The doctor's competence, authority, and persuasiveness
determine patient contact, the degree of trust in the doctor, and the success of treatment.
The doctor should be able to correctly assess the mental state of patients. Often it is
necessary to consult with psychiatrists, neurologists, and vegetologists to make a diagnosis
and select adequate psychotropic therapy. Intervention in these areas by non-specialists can
cause additional trauma to the patient and drive him away from the doctor.
Diet therapy. The patient is prescribed an exclusion diet that does not contain caffeine,
lactose, fructose, sorbitol, vinegar, alcohol, pepper, smoked products, as well as products
that cause excessive gas formation. Traditionally, patients with predominant constipation
are recommended to follow a plant -based diet.
Primary course of treatment. The key point in the diagnosis of IBS is to conduct a
primary course of treatment with subsequent reassessment of diagnosis. The purpose of
such treatment is to eliminate the symptoms of the disease and check ex juvantibus the
correctness of the diagnosis, the absence of the need for further search for organic
pathology and the implementation of additional diagnostic procedures. As a result of
treatment, the patient should make sure that his condition is improving or at least not
getting worse, which makes it possible to make a decision with greater confidence and in
agreement with the patient not to conduct further follow-up.
Treatment of patients with predominant pain and flatulence. The defining symptom of
the disease is pain, the relief of which in many patients is accompanied by a decrease in
the severity of diarrhea, constipation, bloating. For patients with pain and flatulence, there
is no standardized treatment regimen or drug of choice that has proven effective in studies
under the protocol based on long -term follow-up results. There is a large selection of
drugs of various pharmacological groups that can be used for the pain form of IBS:
1)3-M3a-anticholinergic agents - hyoscinebutyl bromide; 2) cholecystokinin antagonists
-loxiglumide; 3)somatostatin analogues; 4) 5-hydroxytryptamine 3-ondansetron
antagonists; 5) myotropic antispasmodics (mebeverine hydrochloride, otilonium bromide
and pinoveriuma bromide). It is considered optimal to prescribe pinoverium bromide, 50
mg 3 times a day, both for the duration of the primary course of treatment and as a basic
therapy. Pinoverium bromide provides an effective antispasmodic effect in 90% of
patients, relieves abdominal pain, and reduces the severity of flatulence. By its mechanism
of action, the drug belongs to the selective blockers of L-1,2-potential-dependent calcium
channels of the intestinal smooth muscle, which ensures the absence of vasodilator and
antiarrhythmic effects inherent in other calcium channel blockers.
The latest medicines should include: 1) k-opiate receptor agonistsто; 2)
5-hydroxytryptamine antagonists4; 3) adrenergic substances (k2 - drugs);
4) antagonists of substance P.
Special tactics are required when relieving intense abdominal pain. Even with a
previously established diagnosis of IBS, symptoms of "acute abdomen" are excluded
based on the results of examination, palpation, rapid blood tests, ultrasound and an
overview image of the abdominal band, after which parenteral antispasmodic drugs
(giacinbutyl bromide, platifillin , etc.) can be used.
Treatment of patients with predominant diarrhea. One of the most severe symptoms of
IBS, which inevitably affects the quality of life of patients, is diarrhea, which must be
eliminated as soon as possible. Diarrhea is the most common cause of temporary disability
in IBS.
Loperamide (imodium) is recognized as the drug of choice for the treatment of
diarrheal IBS. In 50% of patients, symptoms disappear after taking the first dose of the
drug and in 87% - after 12-24 hours from the start of treatment. Loperamide belongs to the
agonists οφ μ- opiate receptors, which determinesеits ability to suppress rapid propulsive
contractions of the intestine, leading to a slowdown in the transit of fecal masses. This is
accompanied by a decrease in the passage of the liquid part of the chyme, increases the
absorption of liquid and electrolytes. Other equally important mechanisms of action of
loperamide in IBS include a decrease in the susceptibility of the rectal wall to stretching,
which makes it possible to increase the pain perception threshold, soften and eliminate
tenesmus. Loperamide is known to increase the tone of anal sphincters, which helps to
improve the control of bowel movements. In patients with chronic functional diarrhea in
patients with IBS, the initial dose of loperamide for tall adults is 4 mg (2capsules). The
maintenance dose should not exceed the maximum allowable daily dose for adults-16 mg
(8 capsules). In this case, the chair should be no more than 3 times a day. If there is no
stool and normal stool occurs within 12 hours, treatment should be discontinued. The drug
does not penetrate the blood-brain barrier and does not have a central narcotic effect.
When соблюдении these dosages are observed, loperamide is safe, does not cause side
effects, and therefore is included in the group of over-the-counter medications.
Combination drug containing loperamide and simethicone - a substance that
absorbs gases, which is especially desirable for IBS-has also proven itself well in IBS.
If the patient has a slight increase in the frequency of stool, it is possible to use
adsorbents-calcium carbonate, activated carbon, dysmectite 3 g per day in the form of a
suspension. However , it should be remembered that the antidiarrheal effect of these drugs
occurs no earlier than in 3-5 days.
In patients with psychopathological disorders, a short course of tricyclic antidepressants
or anxiolytics can relieve abdominal pain and concomitant diarrhea due to the
anticholinergic properties of the drugs.
Treatment of patients with predominant constipation. With constipation, if there is no
effect from dietary measures, they resort to prescribing osmotic laxatives, among which
lactulos, magnesia milk, macrolgol 4000 2 sachets 2 times a day, etc. have proven
themselves best. In case of persistent constipation, the next step may be to add prokinetics,
primarily cisapride at a dose of 5-10 mg H-4 times a day. The use of surfactant laxatives,
especially saline ones, should be avoided, as they can increase the pain syndrome. When
the pain syndrome is combined with constipation, the use of tricyclic antidepressants
andanxiolytics can increase constipation, flatulence , and pain.
Unsatisfactory treatment results make it necessary to use various additional treatment
procedures - physical therapy, physiotherapy, hypnotherapy, methods based on the
principle of biofeedback, and group interpersonal treatment in special schools and clubs
for patients with IBS.
The effectiveness of the program is determined not so much by the subjective state and
complaints, but by the improvement of the patient's psychosocial state and quality of life.
It is essential that the assessment of the effectiveness of treatment programs in general and
the effect of individual drugs in their trials, according to the Rome Consensus, should be
given by the patient himself.
Diagnosis and treatment of diseases manifested by gastric dyspepsia

Organic gastric dyspepsia is observed in diseases of the stomach, duodenum, gallbladder, liver
and pancreas. This publication will cover in detail gastric and duodenal ulcers, symptomatic
gastroduodenal ulcers, chronic gastritis, stomach cancer, functional (non-ulcerative) dyspepsia,
cholelithiasis, and chronic pancreatitis.

Peptic ulcer of the stomach and duodenum

Peptic ulcer disease is a chronic recurrent disease that occurs with alternating periods of
exacerbation and remission, the main sign of which is the formation of a defect (ulcer) in the
wall of the stomach and duodenum, which penetrates – in contrast to superficial damage to the
mucous membrane (erosions) – into the submucosal layer.

The prevalence of peptic ulcer disease among the adult population varies from 5 to 15% in
different countries (on average, 7-10%). Duodenal ulcers are 4 times more common than gastric
ulcers. Among patients with duodenal ulcers, men significantly predominate over women, while
among patients with gastric ulcers, the ratio of men to women is approximately the same. In
recent years, there has been a tendency to reduce the number of hospitalized patients with an
uncomplicated course of peptic ulcer disease, but to increase the frequency of ulcerative bleeding
due to the increasing use of nonsteroidal anti-inflammatory drugs (NSAIDs).

Etiology and pathogenesis

According to modern concepts, the pathogenesis of peptic ulcer disease in general is reduced to a
violation of the balance between the factors of acid-peptic aggression of gastric contents and
elements of protection of the gastric mucosa and duodenum.

Aggressive factors include increased production of hydrochloric acid (as a result of an increase
in the mass of lining cells, hyperproduction of gastrin, disorders of the nervous and humoral
regulation of hydrochloric acid secretion), increased production of pepsinogen and pepsin
formation, disorders of gastric and duodenal motility (delay or acceleration of evacuation of
acidic contents from the stomach), direct traumatic effect of food.

The following factors lead to a weakening of the protective factors of the gastric mucosa and
duodenum: a decrease in the production and violation of the qualitative composition of gastric
mucus, a decrease in the production of bicarbonates, a deterioration in the processes of
regeneration and blood flow in the mucous membrane, a decrease in the content of
prostaglandins in the stomach wall.

A certain place in the pathogenesis of peptic ulcer disease is also occupied by hormonal factors
(sex hormones, adrenal cortex hormones, gastro-intestinal peptides), biogenic amines (histamine,
serotonin, catecholamines), immune mechanisms, and disorders of lipid peroxidation processes.

Currently, it is established that the most important role in enhancing the aggressive properties of
gastric contents and weakening the protective properties of the gastric mucosa and duodenum is
played by the microorganisms Helicobacter pylori (H. pylori), discovered in 1983 by Australian
scientists B. Marshall (B. Marshall) and J. Smith. By J. Warren. These microorganisms are
detected in 90-95% of patients with duodenal ulcers and in 70-85% of patients with gastric
ulcers.

The spectrum of adverse effects of H. pylori on the gastric mucosa and duodenum is quite
diverse. These bacteria produce a number of enzymes (urease, protease, phospholipase) that
damage the protective barrier of the mucous membrane, as well as various cytotoxins. The most
pathogenic strains are VacA, a strain of H. pylori that produces vacuolating cytotoxin, leading to
the formation of cytoplasmic vacuoles and death of epithelial cells, and CagA, a strain that
expresses a gene associated with cytotoxin. This gene encodes a 128 kDa protein that has a direct
damaging effect on the gastric mucosa. H. pylori promotes the release of interleukins, lysosomal
enzymes, and tumor necrosis factor in the gastric mucosa, which causes the development of
inflammatory processes in the gastric mucosa.

Contamination of the gastric mucosa with H. pylori is accompanied by the development of

superficial antral gastritis and duodenitis and leads to an increase in the level of gastrin and a
decrease in the level of somatostatin, followed by increased secretion of hydrochloric acid. An
excessive amount of hydrochloric acid entering the duodenal lumen, in conditions of a relative
deficiency of pancreatic bicarbonates, contributes to the progression of duodenitis and, in
addition, causes the appearance in the duodenum of areas of gastric metaplasia (reconstruction of
the epithelium of the duodenal mucosa according to the gastric type), which are quickly
populated H.pylori. In the future, with an unfavorable course, especially in the presence of
additional etiological factors (hereditary predisposition, 0 (1) blood type, smoking, neuropsychic
stress, alimentary errors, taking ulcerogenic drugs, etc.), an ulcer defect is formed in the areas of
the metaplastic gastric mucosa.

In 5-10% of patients with duodenal ulcers and 15-20% of patients with gastric ulcers, the
development of the disease can occur without the involvement of H. pylori. First of all, this
applies to symptomatic gastroduodenal ulcers.

Classification

There is no generally accepted classification of peptic ulcer disease. From the point of view of
nosological isolation, peptic ulcer disease and symptomatic gastroduodenal ulcers are
distinguished, as well as peptic ulcer disease associated and not associated with H. pylori.

Depending on the localization, gastric ulcers (cardiac and subcardial divisions, gastric body,
antrum, pyloric canal), duodenal ulcer (bulb and postbulbar division), as well as combined ulcers
of the stomach and duodenum are distinguished. In this case, ulcers can be located on the small
or large curvature, anterior and posterior walls of the stomach and duodenum.

According to the number of ulcerative lesions, single and multiple ulcers are distinguished, and
depending on the size of the ulcer defect – ulcers of small (up to 0.5 cm in diameter), medium
(0.6–1.9 cm in diameter) sizes, large (2.0–3.0 cm in diameter) and giant (over 3.0 cm in
diameter) ulcers.

The diagnosis indicates the stage of the disease: exacerbation, scarring (endoscopically
confirmed stage of "red" and "white" scarring) and remission, as well as the presence of
cicatricial and ulcerative deformity of the stomach and duodenum.
When making a diagnosis of peptic ulcer, complications of the disease (bleeding, perforation,
penetration, perigastritis and periduodenitis, cicatricial and ulcerative stenosis of the pylorus) are
indicated, including anamnestic, as well as operations performed for peptic ulcer.

Clinical picture

The leading symptom of peptic ulcer exacerbation is pain in the epigastric region, which can
radiate to the left half of the chest and the left scapula, thoracic or lumbar spine. Pain occurs
immediately after eating (with ulcers of the cardiac and subcardial parts of the stomach), half an
hour or an hour after eating (with ulcers of the stomach body), With ulcers of the pyloric canal
and duodenal bulb, late pain is usually observed (2-3 hours after eating), hunger pains that occur
on an empty stomach and pass after eating, and also night pains. Pain passes after taking
antacids, antisecretory and antispasmodic drugs, and applying heat.

With an exacerbation of peptic ulcer disease, dyspeptic disorders are often found: acid belching,
heartburn, nausea, constipation. A characteristic symptom is vomiting of acidic gastric contents,
which occurs at the height of pain and brings relief, and therefore patients can cause it
artificially. However, currently this symptom is not so common.

Typical peptic ulcer diseases are seasonal (spring and autumn) periods of increased pain and
dyspeptic disorders. When the disease worsens, weight loss is often noted, because, despite the
preserved appetite, patients limit themselves to food, fearing increased pain.

You should also consider the possibility of an asymptomatic course of peptic ulcer
disease. According to some reports, the frequency of such cases can reach 30%.

Palpation and percussion of the abdomen with uncomplicated peptic ulcer disease reveals the
following symptoms:

• moderate, and in the period of exacerbation pronounced pain in the epigastrium, as a rule,
localized. With a stomach ulcer, soreness is localized in the epigastrium along the midline or on
the left, with a duodenal ulcer-more on the right;

• percussion soreness is a symptom of Mendel. This symptom is detected by abrupt percussion

with a finger bent at a right angle over symmetrical areas of the epigastric region. According to
the localization of the ulcer, local, limited soreness appears with such percussion. Sometimes the
soreness is more pronounced on inspiration. Mendel's symptom usually indicates that the ulcer is
not limited to the mucous membrane, but is localized within the wall of the stomach or
duodenum with the development of a periprocess;

• local protective tension of the anterior abdominal wall, more characteristic of duodenal ulcers
during exacerbation of the disease. The origin of this symptom is explained by irritation of the
visceral peritoneum, which is transmitted to the abdominal wall by the mechanism of the
viscero-motor reflex. As the exacerbation stops, the protective tension of the abdominal wall
progressively decreases.

Course and complications

In uncomplicated cases, peptic ulcer disease usually occurs with alternating periods of
exacerbation of the disease (lasting, on average, from 3-4 to 6-8 weeks) and remission (lasting
from several months to several years). Under the influence of adverse factors (for example,
physical overexertion, alcohol abuse, taking ulcerogenic medications, etc.), complications may
develop. These include bleeding, perforation and penetration of the ulcer, the development of
perivisceritis, the formation of cicatricial-ulcerative stenosis of the pylorus, the occurrence of
malignancy of the ulcer.

Ulcerative bleeding is observed in 15-20% of patients with peptic ulcer disease, more often with
gastric localization of ulcers. It is manifested by vomiting of "coffee grounds" (hematemesis) or
black tarry stools (melena). With massive bleeding and low secretion of hydrochloric acid, as
well as the localization of ulcers in the cardiac part of the stomach, an admixture of unchanged
blood may be noted in the vomit. Sometimes the first place in the clinical picture of ulcerative
bleeding is taken by general complaints (weakness, loss of consciousness, decreased blood
pressure, tachycardia), while melena may appear only after a few hours.

Perforation (perforation) ulcers occur in 5-15% of patients with peptic ulcer disease, more often
in men. Physical overexertion, alcohol intake, and overeating are predisposed to its
development. Sometimes the perforation occurs suddenly, against the background of an
asymptomatic ("silent") course of peptic ulcer disease. Perforation of the ulcer is clinically
manifested by acute ("dagger") pain in the epigastric region, the development of a collaptoid
state. Examination of the patient reveals" board-like " muscle tension of the anterior abdominal
wall and sharp pain on palpation of the abdomen, a positive Shchetkin-Blumberg symptom. In
the future, sometimes after a period of imaginary improvement, the picture of diffuse peritonitis
progresses.

Penetration is understood as the penetration of a gastric ulcer or duodenal ulcer into surrounding
tissues: the pancreas, omentum minor, gallbladder, etc. When the ulcer penetrates, persistent
pains appear that lose their former connection with food intake, body temperature rises, and an
increase in ESR is detected in blood tests. The presence of ulcer penetration is confirmed
radiologically and endoscopically.

Perivisceritis refers to the adhesive process that develops in peptic ulcer disease between the
stomach or duodenum and neighboring organs (pancreas, liver, gallbladder). Perivisceritis is
characterized by more intense pain, which increases after a large meal, with physical exertion
and concussion of the body, sometimes an increase in temperature and an acceleration of
ESR. Radiologically and endoscopically, deformities and limited mobility of the stomach and
duodenum are detected.

Pyloric stenosis is usually formed after scarring of ulcers located in the pyloric canal or the
initial part of the duodenum. Often, the development of this complication is facilitated by the
operation of suturing a perforated ulcer in this area. The most characteristic clinical symptoms of
pyloric stenosis are vomiting of food eaten the day before, as well as belching with the smell of
"rotten" eggs. Palpation of the abdomen in the epigastric region can reveal a " late splashing
noise "(Vasilenko's symptom), sometimes gastric peristalsis becomes visible. With
decompensated pyloric stenosis, patients ' exhaustion may progress, and electrolyte disturbances
may occur.
Malignancy (malignancy) of a benign ulcer is not as frequent a complication of gastric ulcers as
previously thought. Malignancy of the ulcer is often mistaken for cases of timely unrecognized
infiltrative-peptic ulcer cancer of the stomach. Diagnosis of ulcer malignancy is not always
easy. Clinically, it is sometimes possible to note a change in the course of peptic ulcer disease
with a loss of frequency and seasonality of exacerbations. Blood tests reveal anemia, increased
ESR. The final conclusion is made during histological examination of biopsies taken from
various parts of the ulcer.

Diagnostics

During the period of exacerbation of peptic ulcer disease, an objective study often reveals pain in
the epigastric region on palpation, combined with moderate resistance of the muscles of the
anterior abdominal wall. There may also be local percussion soreness in the same area (Mendel's
symptom), but these signs are not strictly specific for exacerbation of peptic ulcer disease.

A clinical blood test for an uncomplicated course of peptic ulcer disease most often remains
without significant changes. Sometimes there is a slight increase in the content of hemoglobin
and red blood cells, but anemia can also be detected, indicating obvious or hidden
bleeding. Leukocytosis and ESR acceleration occur in complicated forms of peptic ulcer disease
(with ulcer penetration, pronounced perivisceritis).

A certain place in the diagnosis of exacerbations of peptic ulcer disease is occupied by the
analysis of feces for hidden blood. When interpreting its results, it should be remembered that a
positive reaction to latent blood occurs in many other diseases, which requires their mandatory
exclusion.

All patients need a general blood test, urine, feces, and a biochemical blood test (total protein,
albumin, bilirubin, glucose, cholesterol, amylase, lipase, serum iron, and transaminases).

An important role in the diagnosis of peptic ulcer disease is played by the study of the
acid-forming function of the stomach, which is carried out using fractional gastric sounding or
pH-metry (in recent years – using daily monitoring of intragastric pH). With ulcers of the
duodenum and pyloric canal, increased (less often – normal) indicators of acid production are
usually noted, with ulcers of the stomach body and subcardial region – normal or
reduced. Detection and confirmation of histamine-resistant achlorhydria almost always precludes
the diagnosis of duodenal ulcer and casts doubt on the benign nature of the gastric ulcer.

The main importance in the diagnosis of peptic ulcer disease are X-ray and endoscopic methods
of research.

During X-ray examination there is a direct sign of peptic ulcer disease – a "niche" on the contour
or relief of the mucous membrane and indirect signs of the disease (local circular spasm of
muscle fibers on the opposite wall of the stomach in the form of a "pointing finger" in relation to
the ulcer, convergence of the folds of the mucous membrane to the "niche", cicatricial-ulcerative
deformity of the stomach and duodenal bulb, hypersecretion on an empty stomach, disorders of
gastroduodenal motility).

Endoscopic examination confirms the presence of an ulcer defect, specifies its localization,

depth, shape, size, allows you to assess the condition of the bottom and edges of the ulcer,
identify concomitant changes in the mucous membrane, violations of gastroduodenal
motility. When the ulcer is located in the stomach, a biopsy is performed, followed by a
histological examination of the obtained material, which makes it possible to exclude the
malignant nature of the ulcerative lesion.

To exclude the pathology of the hepatobiliary system and pancreas, ultrasound of the abdominal
organs is mandatory.

To determine further treatment tactics, the results of a study of the presence of H. pylori in the
gastric mucosa, which can be carried out by various methods, are extremely important.

Serological method (sensitivity and specificity of 90%), which detects antibodies to H. pylori

(most often now the method of enzyme-linked immunosorbent assay is used) is mainly used for
screening studies to detect infection in various population groups, since it does not require
endoscopy, complex devices, or specially trained personnel. This method is not suitable for
monitoring the effectiveness of eradication therapy, since the change in the titer of
anti-helicobacter antibodies occurs several months after eradication. In recent years, serological
methods have been developed to identify pathogenic strains of H. pylori.

Microbiological (bacteriological) method (sensitivity 80-90%, specificity 95%) the preparation

of H. pylori culture has the advantage that it can be used to determine the sensitivity of
microorganisms to a particular antibacterial drug. However, this method is quite expensive. In
addition, it is associated with certain difficulties due to the need for special environments,
optimal temperature, humidity, atmospheric air quality, etc. This leads to the fact that the growth
of colonies of microorganisms can not always be obtained. The disadvantage of this method is
also due to the fact that its results usually have to wait at least 10-14 days. In clinical practice, it
is mainly used in cases of H. pylori infection that is resistant to conventional antihelicobacteric
therapy regimens.

Morphological (histological) method (sensitivity and specificity of 90%) is currently-along with

the rapid urease test-one of the most common methods for the primary diagnosis of H. pylori
infection. Examination of biopsies of the gastric mucosa using various colors (acridine orange,
Giemsa dye. silvering according to Wartin-Starry) allows not only to detect the presence of H.
pylori with a high degree of reliability, but also to quantify the degree of contamination.

Biochemical methods, Of these, the most commonly used rapid urease test is currently the most
popular in the primary diagnosis of H. pylori infection. The rapid urease test (CLO-test and
Campy-test are widely used in clinical practice; sensitivity and specificity are 90%) is based on
the determination of changes in the pH of the medium by the color of the indicator, which occurs
as a result of the release of ammonia during the cleavage of urea by bacterial urease. The results
of this test become known as early as 1 hour after receiving biopsies of the gastric mucosa. In
addition, the urease test is the cheapest of all methods for diagnosing H. pylori infection (only
the method for diagnosing H. pylori in smears-prints, which is not currently used due to low
sensitivity, is cheaper than this test). The disadvantages of the method include the fact that its
results become false negative when the number of H. pylori microorganisms in the biopsy
sample is less than 104, in this connection, it can give erroneous conclusions when monitoring
the completeness of eradication. When using endoscopic methods for the diagnosis of H. pylori,
at least 2 biopsies are taken from the stomach body and 1 biopsy from the antrum. The reliability
of the results increases if one patient uses not one, but two diagnostic methods (for example, the
morphological method and the rapid urease test).

Radionuclide methods, the most famous of which is considered to be a breath test (sensitivity

95%, specificity 100%) using urea labeled with isotopes 13With or 14C, suggest the use of a mass
spectrograph to capture these isotopes in exhaled air. Abroad, the breath test is considered the
"gold standard" for monitoring the completeness of eradication therapy, since it is non-invasive
and highly sensitive. In Russia, the respiratory urease test has become available thanks to
domestic developments; at the same time, the analysis of the isotopic ratio of 13with2/12with2 It is
performed using the original diode laser spectroscopy.

In 1998, a non-invasive method for determining the H. pylori antigen in feces using
enzyme-linked immunosorbent assay was proposed, which can also be used to control the
eradication of infection.

Determination of H. pylori DNA (in the gastric mucosa, saliva, etc.) by polymerase chain
reaction (PCR)is becoming increasingly widespread. This is the most accurate method of
diagnosing H. pylori infection to date, especially in cases where the bacteria acquire a coccoid
shape (for example, after a course of antibacterial therapy) and when other diagnostic methods
(in particular, the rapid urease test) give false negative results. An original Russian development
allows the use of PCR for non-invasive determination of H. pylori in feces.

Maastricht-3 (the latest consensus on the treatment of H. pylori infection in 2005) emphasizes
that the main tests for the diagnosis of H. pylori should be: 13With MSD (mass spectrographic
breath test) and antigenic fecal, although in certain situations (with a bleeding ulcer, atrophic
gastritis, MALT-lymphoma and the use of PPIs) serology has the advantage. A rapid urease test
and its positive results are sufficient grounds for the use of first-line H. pylori
eradication. Determination of antibodies in urine or saliva is possible only with extensive
epidemiological studies. Confirmation of eradication should be carried out no earlier than in 4
weeks, if possible-with the help of 13With MDT, and if it is unavailable - by determining the fecal
antigen of H. pylori.

Differential diagnosis

Peptic ulcer disease should be differentiated from symptomatic ulcers of the stomach and
duodenum, the pathogenesis of which is associated with certain background diseases or specific
etiological factors (for example, with the use of NSAIDs). Symptomatic gastroduodenal ulcers
(especially medicinal ones) often develop acutely, sometimes manifested by sudden
gastrointestinal bleeding or perforation of ulcers, occur with atypical clinical manifestations
(erased picture of exacerbation, lack of seasonality and periodicity).

Gastroduodenal ulcers in Zollinger-Ellison syndrome differ from the usual peptic ulcer disease in
extremely severe course, multiple localization (often even in the jejunum), persistent
diarrhea. When examining such patients, there is a sharply increased level of gastric acid
excretion (especially in basal conditions), an increased content of gastrin in the blood serum is
determined (3-4 times compared to the norm). Provocative tests (with secretin, glucagon, etc.)
and ultrasound examination of the pancreas help to recognize
Zollinger-Ellison syndrome. Gastroduodenal ulcers in patients with hyperparathyroidism differ
from peptic ulcer disease (in addition to a severe course, with frequent relapses, a tendency to
bleeding and perforation) by the presence of signs of increased parathyroid gland function
(muscle weakness, bone pain, thirst, polyuria). The diagnosis is made on the basis of studying
the content of calcium and phosphorus in the blood serum, identifying signs of hyperthyroid
osteodystrophy, characteristic symptoms of kidney damage and neurological disorders.

If ulcerative lesions are found in the stomach, it is necessary to make a differential diagnosis
between benign ulcers, malignancy of the ulcer and primary ulcerative form of gastric
cancer. The malignant nature of the lesion is supported by its very large size (especially in young
patients), the localization of the ulcerative defect on the large curvature of the stomach, the
presence of an increase in ESR and histamine-resistant achlorhydria. During X-ray and
endoscopic examination in cases of malignant gastric ulcers, the irregular shape of the ulcer
defect, its uneven and irregular shape are revealed. lumpy edges, infiltration of the gastric
mucosa around the ulcer, rigidity of the stomach wall at the site of ulceration. Endoscopic
ultrasonography can be of great help in assessing the nature of damage to the stomach wall at the
site of ulceration, as well as the state of regional lymph nodes. The final conclusion about the
nature of the ulcer lesion is made after histological examination of ulcer biopsies. Taking into
account the possibility of false negative results, the biopsy should be repeated until the ulcer is
completely healed, with at least 3-4 pieces of tissue taken at each examination.

Peptic ulcer treatment

Indications for hospitalization: peptic ulcer disease with a clinical picture of severe exacerbation
(severe pain syndrome); detection of ulcers in the stomach that require differential diagnosis
between benign ulcers and stomach cancer; signs of gastrointestinal bleeding (melena, vomiting
of blood, etc.), perforation and penetration of the ulcer defect; gastric ulcer and duodenal ulcer
with complications in the anamnesis; peptic ulcer disease with concomitant diseases.

Gastric and duodenal ulcers scar in almost all cases, if during the day it is possible to maintain
the level of intragastric pH>3 for about 18 hours. As you know, this rule is met only by PPI (nor
N2- blockers, nor selective cholinolytics, nor, moreover, antacids can not perform it), which
explains why drugs of this group are most effective in the treatment of peptic ulcer disease.

Antisecretory drugs (currently most commonly used for this purpose PPI) are a means of basic
therapy for exacerbation of peptic ulcer disease; they are prescribed to relieve pain and dyspeptic
disorders, as well as to achieve scarring of the ulcer defect in the shortest possible time.

Currently, there is a strict protocol for pharmacotherapy of peptic ulcer exacerbation, which
provides for the appointment of the selected drug in a certain dose: rabeprazole-at a dose of 20
mg per day, omeprazole-at a dose of 20 mg per day, lansoprazole-30 mg per day,
pantoprazole-40 mg per day. The duration of treatment is determined by the results of
endoscopic monitoring, which is carried out at two-week intervals (i.e. after 2, 4, 6, 8 weeks).

An important point in modern pharmacotherapy of peptic ulcer disease is the absence of

fundamental differences in approaches to the treatment of gastric ulcers and duodenal ulcers. For
a long time, it was believed that duodenal ulcers require prescribing antisecretory drugs, and
gastric ulcers require drugs that stimulate regeneration processes. It is now generally accepted
that after confirmation of the benign nature of gastric ulcers, the treatment of these patients is
carried out in the same way as the treatment of patients with duodenal ulcers. The only difference
is the duration of the course of pharmacotherapy. Given that gastric ulcers scar more slowly than
duodenal ulcers, the control of gastric ulcer scarring is carried out not after 4 and 6 weeks, as in
duodenal ulcers, but, respectively, 6 and 8 weeks after the start of taking medications. On
average, the rate of scarring of gastric ulcers is 0.5 cm in 10-12 days, and duodenal ulcers-0.5 cm
per week. The rate of scarring depends on age, the presence of concomitant pathology of the
respiratory system, blood circulation (tissue regeneration decreases), and the endocrine system
(especially in diabetes mellitus).

Peptic ulcer maintenance pharmacotherapy protocol

The main problem of conservative treatment of peptic ulcer disease is, as is known, the high rate
of ulcer recurrence after discontinuation of the course of treatment for exacerbation of the
disease, which averages 70% during the first year after the ulcer scarring is achieved. This fact
served as the basis for the development of maintenance pharmacotherapy regimens prescribed to
patients after the end of the course of treatment.

Extensive experience has been accumulated in the use of daily maintenance (half) doses of PPIs
for anti-relapse therapy, which reduce the incidence of peptic ulcer relapses within a year by up
to 15%. Later, continuous maintenance of PPIs was replaced by intermittent maintenance
pharmacotherapy regimens. These include " supportive self-treatment "or "on-demand" therapy,
where patients themselves determine the need for medication based on their state of health, and
so on. "weekend treatment", when the patient remains without treatment from Monday to
Thursday and takes antisecretory drugs from Friday to Sunday inclusive. The effectiveness of
maintenance intermittent pharmacotherapy is inferior to that with daily medication; the
frequency of exacerbations of peptic ulcer disease on its background is 30-35%.

Currently, when the implementation of eradication antihelicobacter therapy is recognized as the

cornerstone of anti-relapse treatment of peptic ulcer, the indications for maintenance
pharmacotherapy with antisecretory drugs have significantly narrowed. It is considered
necessary in patients who have peptic ulcer disease without contamination of the gastric mucosa.
Pylori (these are 15-20% of patients with gastric ulcers and about 5% of patients with duodenal
ulcers), in patients who have failed at least 2 attempts at anthelicobacter treatment, as well as in
patients with a complicated course of the disease (in particular, if there is a history of perforation
of ulcers).

Eradication therapy schemes

First-line therapy-triple therapy (7 days):

1. Standard dose of one of the PPIs: omeprazole (2 × 20 mg), lansoprazole (2 × 30 mg),

pantoprazole (2 × 40 mg), rabeprazole (2 × 20 mg), esomeprazole (2 × 20 mg);

2. Clarithromycin 500 mg 2 times a day.

3. Amoxicillin 1000 mg 2 times a day /or metronidazole 400 or 500 mg 2 times a day.

Second-line therapy-quadrotherapy (7 days):

1. Bismuth subcitrate 100 mg 4 times a day or bismuth subsalicylate 600 mg 4 times a day.
 2. Standard dose of one of the PPIs: omeprazole (2 × 20 mg), lansoprazole (2 × 30 mg),
pantoprazole (2 × 40 mg), rabeprazole (2 × 20 mg), esomeprazole (2 × 20 mg);

3. Metronidazole 500 mg 3 times a day;

4. Tetracycline 500 mg 4 times a day;

In regions where the level of metronidazole resistance exceeds 40%, amoxicillin is used in the
first line, and in regions with low metronidazole resistance, metronidazole can be used. Triple
therapy for 14 days compared to seven-day triple therapy allows you to increase the effectiveness
of

the level of eradication increased by about 12% (Maastricht-3, 2005). Studies have shown that
the average level of H. pylori resistance to clarithromycin in Europe is at the level of 9.8% (in
the south of Europe-18.8%, in the north-about 4%, in the center of it-about 9%). In
clarithromycin-sensitive patients, the level of H. pylori eradication is 87.8%, and in
clarithromycin-resistant patients, it does not exceed 30%. These data led to the conclusion that
clarithromycin should not be used if the resistance to it exceeds 15-20%. Therefore, in countries
with high clarithromycin resistance and high metronidazole resistance it is preferable to
immediately prescribe quadrotherapy as the first line of treatment. The most effective second line
of treatment is classical quadrotherapy, based on the use of bismuth. In cases of unsuccessful
eradication and second-line treatment, the following "rescue therapy” options are
considered: PPIs + amoxicillin in high doses (3 g / day) for 10-14 days; PPIs + amoxicillin +
rifabutin (or levofloxacin) for 7-10 days; PPIs + bismuth + tetracycline + furazolidone for 7
days.

The best method is laboratory testing for H. pylori resistance. This study should be applied
whenever possible.

According to the Maastricht-3 consensus, H. pylori is the most proven risk factor for non-cardiac
gastric cancer (level of evidence A). Non-cardiac adenocarcinoma is associated with H. pylori in
an average of 71% of cases. H. pylori eradication prevents the development of preneoplastic
changes in the gastric mucosa, if it is reached before the hypothetical "point of no return". H.
pylori eradication to prevent gastric cancer is cost-effective, although further global research is
needed.

Treatment tactics in case of ineffectiveness of conservative therapy

The ineffectiveness of conservative treatment of patients with peptic ulcer disease can manifest
itself in two variants: a frequently recurrent course of peptic ulcer disease (i.e., with a frequency
of exacerbations more than 2 times a year) and the formation of refractory gastroduodenal ulcers
(ulcers that do not scar during 12 weeks of continuous treatment).

Factors that determine the frequently recurrent course of peptic ulcer disease are contamination
of the gastric mucosa with H. pylori microorganisms, taking NSAIDs, the presence of a history
of ulcerative bleeding and perforation of the ulcer, as well as low " compliance "(compliance),
i.e. the patient's lack of willingness to cooperate with the doctor, manifested in the refusal of
patients to stop smoking and alcohol consumption, their irregular medication intake. Therefore,
measures that increase the effectiveness of treatment of patients with frequently recurrent peptic
ulcer disease include: H. pylori eradication, which reduces the rate of ulcer recurrence within a
year from 70% to 4-5% and also reduces the risk of repeated ulcerative bleeding, prescribing
long-term maintenance therapy with antisecretory drugs in cases of non-H. pylori peptic ulcer
disease, replacing NSAIDs with paracetamol or selective cyclooxygenase-2 blockers (for
example, celecoxib) as well as prescribing, if necessary, the continuation of NSAID use of the
appropriate "cover" from PPI or misoprostol, increasing the" compliance " of patients (stopping
smoking, alcohol intake, etc.).

Factors contributing to the formation of refractory gastroduodenal ulcers may include the already
mentioned H. pylori infection, NSAID use, low patient "compliance", large and giant ulcers, as
well as the latent Zollinger-Ellison syndrome. Carrying out the above measures, as well as
increasing the dose of PPIs by 2-3 times, a thorough examination of patients in order to exclude
gastrinoma can in many cases successfully solve the problem of refractory ulcers.

Indications for surgical treatment of peptic ulcer disease are currently only complicated forms of
the disease. If all the necessary protocols of conservative treatment are followed, cases of its
ineffectiveness (as an indication for surgery) can be minimized.
 Questions: Diagnosis and differential diagnosis, treatment of various clinical variants of chronic
pancreatitis, pancreatic cancer. Emergency care for acute pancreatitis.
DIFFERENTIAL DIAGNOSIS AND TREATMENT OF
PANCREATIC DISEASES
All diseases of the pancreas are divided into the following groups:
1) inflammatory diseases – acute and chronic pancreatitis.
2) pancreatic cysts;
3) pancreatic tumors.

Chronic pancreatitis (CP) is a chronic inflammatory disease of the pancreas characterized

by the development of diffuse or segmental fibrosis of the gland, and in the periods of
exacerbation - its edema and local necrosis. Long-term course of the disease leads to a
violation of the external secretory and endocrine functions of the pancreas. Numerous
statistical data indicate an increase in the incidence. Thus, in industrially developed
countries, the number of patients with chronic pancreatitis has increased 1.5-2 times over
the past 20 years and amounted to 6.5% of all patients with diseases of the digestive
system. This increase is associated with an increase in alcohol consumption and the
incidence of gallstone disease.
Etiology and pathogenesis. As in acute pancreatitis, biliary-dependent and alcoholic
forms account for 70-80%. Biliary-dependent forms are most often associated with
gallstone disease, especially with small stones and the common bile duct, which, when
they pass into the duodenum, increase pressure in the wirsung duct (pancreatic duct) and
lead to damage to the large duodenal duct. The pathogenetic mechanism of chronic
cholangiogenic pancreatitis is the difficulty of outflow of pancreatic secretions.
Alcoholism is an important cause of the development of CP, but in many cases patients
hide the fact of alcohol abuse from the doctor. Alcohol has a direct toxic effect on the
pancreatic parenchyma, increases the viscosity of pancreatic secretions and the content of
proteins in it, which leads to the formation of protein plugs in the small ducts of the
gland. Protein umbilicals clog the ducts and cause their structural damage, such as duct
dilation and proliferation of their epithelium, stretching of acinar tissue, and focal
atrophy. Protein plugs, calcified, form calcifications. Drug-induced pancreatitis develops
more frequently. Among the drugs that most often damage the pancreas. These include
azathioprine, chlorthizide derivatives, estrogens, furosemide, and tetracycline.
Dysmetabolic forms are observed in hyperparathyroidism, hyperlipidemic syndrome
(familial hypercholesterolemia), hemochromatosis. The infectious origin of CP is likely if
pancreatitis is detected in the replicative phase of viral hepatitis B, when
cytomegalovirus infection and other viral infections are detected. Atherosclerotic
abdominal ischemia and diabetic angiopathy can also cause the development of chronic
pancreatitis, especially in the elderly.

Clinical and morphological variants:

1. Interstitial edematous.
2. Parenchymal.
3. Fibro-sclerotic (indurative).
4. Hyperplastic (pseudotumorous).
5. Cystic.
Clinical picture. Manifestations of pancreatitis are largely determined by the clinical
and morphological variant and phase of the disease.
Interstitial edematous variant, sometimes called subacute, is characterized by
a relatively short history of Rare but significant exacerbations of the disease in the
clinical and laboratory picture resemble acute pancreatitis. Most patients have severe
pain in the upper abdomen, nausea, sometimes vomiting, which does not bring relief,
palpation determines pronounced soreness in the projection PJ. More than 90% of
patients have a significant increase in amylase activity in the blood serum and urine.
At the height of the exacerbation, according to ultrasound and CT, the size of the
gland is usually moderately enlarged. Due to edema of the gland and parapancreatic
tissue, the contours of the organ are not learly formed: its structure is heterogeneous.
As the exacerbation subsides, the size of the pancreas becomes normal, and the
contours become clear. However, in contrast to acute pancreatitis, some of the
morphological changes are stable, for example, areas of moderate pancreatic
compaction are preserved. Incases of exacerbation, complaints are more often
absent, although in some patients the use of fatty, spicy food or alcohol causes
moderate epigastric pain.
The parenchymal variant, also called recurrent, has alonger course (8-10
years). This variant is characterized by alternating periods of exacerbation and
remission. Clinical symptoms in the acute period are less pronounced than in the
interstitial-edematous variant; increased amylase activity in the blood and urine is
less frequent (in 70-80% of cases) and usually does not reach high levels. More than
half of the patients have symptoms of external secretory pancreatic insufficiency:
steatorrhea, polyphalia, and a tendency to diarrhea. According to ultrasound and CT
data, the size and contours of the gland are not significantly changed, the structure is
relatively uniform; there is a stable but uniform compaction of the organ. Changes in
the ductal system in most patients are not detected. During remission, some patients
periodically experience abdominal pain and dyspeptic symptoms.
The fibrosclerotic (indurative) variant usually has a long history. With
diffuse lesion of the gland, intense pain in the upper half of the abdomen is often
observed, sometimes with difficulty yielding to therapy. External secretory
pancreatic insufficiency is observed in almost all patients, and most of them require
constant replacement therapy. Almost all patients have asthenoneurotic syndrome:
rapid exhaustion, low mood, sometimes depressive phenomena, fixation on painful
sensations. It is difficult for many patients to draw a clear line between periods of
exacerbation and remission of the disease. The amylase test in this variant is not very
informative; a moderate increase in amylase activity is observed only in half of the
patients. According to ultrasound and CT data, the size of the pancreas is either
diffusely or locally reduced, the parenchyma is in homogeneously compacted; the
contours are clear, uneven; calcifications are often detected. A number of patients
show signs of dilatation of the pancreatic ducts.
The hyperplastic (pseudotumorous) variant is relatively rare (approximately
in 5% of cases). In most patients, the disease lasts for a long time (more than 10
years). In the upper abdomen, severe, persistent pain occurs. Many patients show
clear signs of external secretory pancreatic insufficiency. Insome cases, it is possible
to feel a painful enlarged area of the gland, similar to a tumor formation. Therapeutic
measures often have little effect on the manifestations of the disease. The amylase
test is positive only in 50-60% of patients. Ultrasound and CT scans reveal
significantly enlarged areas of the gland. Its contours are not even in these areas.
Often it is possible to visualize the expansion of the pancreatic ducts. Differential
diagnosis of this variant with slow-growing pancreatic carcinoma is very difficult.
To clarify the diagnosis, it is necessary to perform repeated ultrasound and CT using
a complete breast biopsy or dynamic monitoring for at least 6-12 months.
 Cystic changes of the pancreas are detected in 10-15% of patients with
pancreatitis. The formation of small (up to 15 mm in diameter) relatively stable cysts
(more precisely, pseudocysts, since they are not lined with epithelium) gives a
certain originality to the course of PC and allows it to be distinguished as a separate
variant. The pain syndrome is more often moderate, although in some patients
during the formation of cysts, the pain reaches high intensity. The amylase test is
positive in almost 90% of patients, with hyperamylasuria occurring 2 times more
often than hyperamylasemia. A prolonged increase in amylase activity in the urine
хаis typical for the formation of pseudocysts. Ultrasound and CT scans reveal a
moderately diffuse or locally enlarged pancreas. Along with liquid formations, there
are inclusions of high density up to calcification. Often, an extension of the ducts
system is detected. In half of cases, the disease occurs with frequent exacerbations.
The effect of conservative treatment у in most patients is positive.
With any variant of the course of chronic pancreatitis, complications may
occur. Violation of the outflow of bile is often short-term in the form of transient
mechanical jaundice. The formation of pseudocysts and abscesses is usually
recorded с by ultrasound and CT. Compression of the portal and splenic veins of the
inflammately altered pancreas is rarely detected. In fact, in severe forms of PH with
a predominant lesion of the body and tail of the gland, subhepatic forms of portal
hypertension develop quite often. Pancreatogenic diabetes mellitus is clinically
manifested only in severe advanced зашедшем pancreatitis, usually proceeds easily
and инсулинотерапии does not require insulin therapy.
Treatment. An important prerequisite for successful treatment of pancreatitis
is the elimination of pathogenic factors. Thus, in alcoholic pancreatitis, the patient
should completely stop drinking alcohol; in bipolar-dependent pancreatitis, a
cholecystectomy should be performed as early as possible after the detection of
calculous cholecystitis and, if necessary, surgery on the biliary tract. Diet is the most
important way to prevent pain and dyspeptic disorders. Patients are very sensitive to
all kinds of dietary disorders. It is recommended to eat within the limits of diet No. 5
with a restriction of fats and taking into account the patient's intolerance to certain
foods and dishes. Food should be taken 4-5 times a day in a warm form. Avoid juicy
and spicy dishes.
Pain management is the most urgent and difficult task. If the pain syndrome
is moderately pronounced, it is sufficient to prescribe a diet, anti - cholinergic drugs
(atropine, platyphylline, gastrocepin) and antispasmodic drugs (no-shpa, papaverine)
inside to relieve pain. Reducing the functional activity of the pancreas and reducing
the intensity of pain contributes to the use of antacids, and if necessary- H2-receptor
blockers or flow pump blockers. With persistent pain syndrome, cholinolytics and
antispasmodics are administered subcutaneously or intramuscularly. Prescribe
injections of analgesics (analgin, baralgin) or narcotic drugs (promedol, fentanyl). In
the absence of an effect, which is usually observed in the indurative and
pseudotumorous variant of pancreatitis, radiation therapy (a single dose of 0.3-0.4
Gy) or high-energy pulsed laser irradiation of the pancreatic region can be used in a
very limited number of cases. For a course of 4-6 irradiations.
External secretory pancreatic insufficiency is usually well compensated by
taking enzyme preparations. Use pancreatin or preparations mezim-forte 10 000,
creon, pancitrate. Especially effective are new enzymatic preparations in which
small pancreatin granules are coated with an anti-acid coating (pancitrate, creon).
Drugs are prescribed depending on the degree of enzymatic insufficiency, 1-3 tablets
during each meal.
When the exacerbation subsides and in the intercostal period, physiotherapy
is prescribed. Hydrotherapy (coniferous, radon and pearl baths) is indicated.
Ultrasound techniques and magnetotherapy are used. The tolerance of thermal
procedures is very individual. In the interventional period, a rational, balanced diet is
recommended with the exclusion of refractory fats, cold fizzy drinks and fresh warm
bread; if signs of external secretory pancreatic insufficiency persist, you should
continue taking enzymatic preparations. Sanatorium-resort treatment is effective
(Essentuki,Leznovodsk , etc.).
Surgical treatment is performed for persistent or frequently recurring diseases
that are resistant to conservative therapy; local complications that do not respond to
conservative therapy (pseudocysts, abscesses, duodenal stenosis, etc.); changes in
протоках the pancreatic ducts that prevent the outflow of pancreatic secretions;
suspected на рак pancreatic cancer.
If false cysts occur, the affected part of the gland is removed, but more often-the
cystostomy. With stenosis of the large duodenal papilla and dilation of the Wirsung
duct, endoscopic or transduodenal papillotomy or longitudinal pancreatojejunostomy
is performed, as well as resection of the gland tail with the formation of a pancreatic
intestinal anastomosis. With biliary -dependent pancreatitis, the best option is to
disconnect the bile duct and pancreatic duct. A promising method is the occlusion of
the pancreatic duct using filling fluids (silicone elastomer SKTN-M, etc.).

Pancreatic cysts are wall-bound accumulations of fluid that form in the

parenchyma of the gland or in the surrounding tissues, which have the
appearance of a sac-like tumor. Cystic changes in the gland a requite common,
but cysts are heterogeneous in their origin.
There are congenital cysts, retention cysts formed as a result of blockage of the
ducts, parasitic cysts, as well as inflammatory and traumatic cysts formed during
tissue breakdown and are pseudocysts, since they are not lined with epithelium.
Cystic formations in the pancreas (pancreas) can be manifestations of cystadenoma
or cystadenocarcinoma.
Congenital cysts should be considered as a malformation. Often, cysts in the
pancreas are combined with cystic lesions of the liver and kidneys.
Cystic fibrosis caused by cystic fibrosis is associated with the release of a
viscous secretion rich in glycoproteins, which clogs the pancreatic ducts. Of the
parasitic cysts, echinococcus is most common.
Pseudocysts have the appearance of cavities formed as a result of the
breakdown of gland tissue when it is damaged or autolysis as a result of
inflammation.
Cystadenomas probably arise as a result of proliferation of the epithelium of
small ducts, since it is this epithelium that lines the cystadenoma walls, while
cystadenocarcinoma develops in malignant fasting.
Symptoms depend on the size, number, location, origin of cysts as well as
their relationship with neighboring organs. With small cysts, symptoms may be
absent for a long time, or with inflammatory pseudocysts, signs of pancreatitis are
noted. In the case of an enlarged cyst, there are constant dull or paroxysmal pains,
which are more often associated with a change in body position than with eating.
When the cyst is located in the glandular head, compression syndrome is observed
(duodenal stenosis, mechanical jaundice). A cyst located in the body and tail of the
pancreas can compress the left ureter, portal vein, and other organs. With secondary
infection of the cyst, involvement of the biliary system in the process, fever,
leukocytosis, and jaundice are observed. Neoplastic cysts have all the signs of a
malignant tumor: infiltrative growth, a tendency to metastasis. An important
objective symptom of a cyst is the probing of the tumor. The pancreatic head cyst is
 palpable at the level of the navel, the body and tail cyst - in the left hypochondrium.
A benign cyst is palpated as a smooth, elastic formation of a round or oval shape. A
malignant cyst is usually irregular in shape, dense, with an uneven surface.
With a decrease in the mass of the functioning parenchyma, signs of exocrine
(maldigestia syndrome) and endocrine (diabetes) insufficiency appear .
Diagnostics.The results of ultrasound examination (ultrasound) and
computed tomography (CT) are crucial in the diagnosis of pancreatic cysts. In these
studies, even small cavities are clearly visible. X-ray examination of the
gastrointestinal tract allows you to clarify the location of the cyst in relation to the
stomach and colon (it can push these organs away). Inflammatory and traumatic
pseudocysts are characterized by prolonged hyperamylasemia and hyperamylasuria.
With an infected cyst, leukocytosis with a rod-shaped shift and an increase in ESR
are observed. A parasitic cyst is characterized by calcification of its capsule and
positive serological tests.
Treatment. For large pancreatic cysts, surgical treatment is performed:
cystectomy or partial resection of the pancreas (radial surgery), external drainage
(application of an external fistula), internal drainage (cisgastrostomy,
cystoduodenostomy or cystojejunostomy).
In case of external secretory and endocrine pancreatic insufficiency
replacement therapy is performed
• control of vascular insufficiency (reopoliglyukin-400-500 ml intravenously,
hydrocortisone-250 mg intramuscularly or intravenously, prednisone -30-60 mg
orally);
• correction of the water-electrolyte composition (500 ml of 0.9% sodium
chloride solution, 500 ml of 5% glucose solution, 20 ml of panangin); liquid and
electrolytes are administered under the control of diuresis (the release of 50 ml of
urine per hour indicates о compensation for the volume of circulating blood).
After the clinical signs subside, treatment is continued for another 1-2 months
according to the principles of treatment of chronic pancreatitis (see chronic
pancreatitis).

Pancreatic cancer is a malignant tumor that develops mainly from the epithelium of small
and minute pancreatic ducts. Factors predisposing to the development of pancreatic
cancer include smoking (the incidence of pancreatic carcinoma in smokers is 2-2.5 times
higher), chronic pancreatitis, and diabetes mellitus (the probability of developing
pancreatic cancer doubles). The risk of developing cancer is increased by exposure to
certain chemicals (such as naphthaolamine), eating high-fat foods, and alcoholism. The
question of the association of excessive coffee consumption with a possible risk of cancer
is discussed.
Classification of pancreatic cancer by stages:
Stage I - the tumor diameter does not exceed 3 cm, there are no metastases.
II stage – a tumor larger than 3 cm, but not extending beyond the organ,
there may be single metastases in nearby regional lymph nodes;
III stage – infiltrative growth of the tumor in the surrounding tissue,
metastases of the tumor in regional lymph nodes;
IVstage – there are distant metastases. In addition, it is customary to divide
cancer by localization: cancer of the head of the pancreas (60-65%), cancer of the
body and tail of the pancreas (30-35%), isolated cancer of the tail of the pancreas (up
to 5%).
Clinical picture. Weight loss, abdominal pain, anorexia and jaundice are
classic symptoms of the disease. Nausea, weakness, fatigue, vomiting, diarrhea and
pain in the spine are also quite common. Weight loss increases rapidly, the patient
loses more than 25% of the original body weight, and this is not always explained
only by anorexia. Pain is observed in 7-90% of patients; with pancreatic head
involvement, pain is more often localized in the epigastric region or in the upper
right quadrant of the abdomen, with tail involvement-in the left hypochondrium.
Pain can be blunt, burning, drilling, and often radiate to the back. A sharp increase in
pain may indicate the growth of the tumor in the retroperitoneal nerve plexus.
Jaundice occurs in 80-90% of patients with a pancreatic head tumor and in
10-40% of patients with lesions of the body and tail. Jaundice increases rapidly and
is accompanied by itching of the skin. Many patients have neuropsychiatric
disorders, insomnia, anxiety, anger, agitation, a feeling of near death, suicidal
intentions. Feel the seal in the depth of the abdominal cavity, which sometimes
transmits aortic pulsation, usually succeeds only with advanced, inoperable cancer,
more often with its localization in the body and tail of the gland. Although the
gallbladder is always enlarged in the presence of jaundice, it can be palpated in
15-40% of cases (Courvoisier's symptom); thrombophlebitis is observed in 10% of
patients with pancreatic cancer, and migrating thrombophlebitis in some cases may
be the first sign of the disease.
Diagnostics. Correct assessment of the clinical picture is of great importance
in the diagnosis of pancreatic cancer. Suspicious signs of pancreatic cancer are:
• age over 50 years.
• unexplained weight loss;
• persistent pain in the upper abdomen, especially with negative results of the
gastrointestinal tract study;
• unexplained pain in the spine;
• relapses of acute pancreatitis that occur without obvious causes:
• signs of exocrine pancreatic insufficiency that appear without obvious reasons;
• sudden development of diabetes mellitus without aggravating circumstances
(obesity, family predisposition to diabetes);
• rapid development of mechanical jaundice without a previous pronounced
pain syndrome;
• migrating thrombophlebitis.
Diagnosis of pancreatic cancer is based on the results of instrumental studies
(ultrasound, CT, EPCG). Ultrasound can detect tumors in the head and body of the
pancreas larger than 2 cm in 70-90% of patients. Smaller tumors, as well as
pancreatic tail tumors, are more difficult to recognize. Based on CT results, the
correct diagnosis of pancreatic cancer can be established in 80% of patients, in
5-10% of cases of proven carcinoma, CT reveals only a diffuse enlargement of the
gland, rather resembling pancreatitis. CT has some advantage over ultrasound, as it
allows you to better visualize the pelvis and tail of the pancreas, as well as adjacent
organs. EPCG reveals narrowing, deviation or obstruction of the main or large
pancreatic ducts in 75-80% of patients, although in some cases the sechanges are
determined earlier than it is possible to detect signs of a tumor using ultrasound and
CT. To verify the diagnosis, if necessary, a targeted biopsy can be performed under
the control of ultrasound or CT. Laboratory biochemical blood tests can only clarify
the nature of jaundice (obturation, parenchymal, hemolytic). The amylase test has no
significant significance in pancreatic cancer; a moderate increase in amylase in the
blood and urine is observed only in 10-20% of patients. Enzyme-linked
immunosorbent assay of tumor markers has expanded the possibilities for
diagnosing pancreatic cancer. The indicators of carbo-hydrate antigen (Ca-19-9) and
 cancer -embryonic antigen (CEA) can be used to assess not only the presence of
pancreatic cancer, but also the possibility of tumor metastases. The level of Ca-19-9
is increased 10-20 times in 80-90% of patients with pancreatic cancer; a sharp
increase in the level of Ca-19-9 or a simultaneous increase in the level of Ca-19-9
and CEA indicates the presence of tumor metastases. A decrease in tumor markers
after radiological surgery indicates a favorable outcome.
Treatment. Until now, pancreatic surgery is rarely performed. Total
pancreatoduodenal resection leads to the development of fatal diabetes, so this
operation is not performed. Usually, a partial pancreatoduodinal resection is
performed with the application of a pancreatic-intestinal anastomosis. In cancer of
the head of the pancreas, resection of the head and part of the body of the gland is
performed, in cancer of the body and tail-resection of the body and tail of the
pancreas together with splenectomy. According to the literature, the proportion of
radical operations does not exceed 18%, postoperative mortality is 10-70%,
depending on the selection of patients and the surgeon's experience. The 5-year
survival rate is not higher than 15%. Chemotherapy with fluororacil (total dose for a
course of 4-5 g) gives a temporary effect only in 15-20% of patients; chemotherapy
(5-fluorouracil, cyclophosphamide, methotrexate, vincristine) – in 20-30% of
patients.

Treatment of non-acute pancreatitis

1
For the treatment of non-severe pancreatitis, it is sufficient to conduct a basic treatment complex:
- hunger,
- probing and aspiration of gastric contents,
- local hypothermia (cold on the stomach),
- analgesics,
- antispasmodics,
- infusion therapy in the amount of up to 40 ml per 1 kg of patient's body weight with forcing of
diuresis within 24-48 hours.
Basic therapy should be enhanced with anti-secretory and anti-enzyme therapy.
2
If there is no effect from basic therapy for 6 hours and at least one of the signs of severe
pancreatitis is present, severe pancreatitis should be detected and the patient should be
transferred to the intensive care unit (intensive care unit) and treated in accordance with severe
acute pancreatitis.
Intensive therapy of severe pancreatitis
The main type of treatment is intensive conservative therapy. At the same time, the basic
complex should be supplemented with a specialized treatment complex, the effectiveness of
which is maximum at an early start of treatment (the first 12 hours from the onset of the disease).
Surgical intervention in the form of laparotomy is indicated for the development of surgical
complications that cannot be eliminated by endoscopic methods (destructive cholecystitis,
gastrointestinal bleeding, acute intestinal obstruction).
Specialized treatment.
 1
Anti-secretory therapy (optimal duration – the first three days of the disease):
- the drug of choice-sandostatin (octreotide) 100 mcg 3 times subcutaneously;
- reserve drugs- kvamatel (40 mg 2 times iv), 5-fluorouracil (5% - 5 ml iv).
2
Rheologically active therapy (heparin, reopoliglukin, refortan).
3
Compensation for plasma loss.
Correction of water-electrolyte and protein losses (in total, at least 40 ml of appropriate infusion
agents per 1 kg of body weight; the ratio of colloidal and crystalloid solutions is 1: 4).
4
Histoprotection:
- anti-enzyme therapy (optimal duration-the first 5 days of the disease;
kontrikal – not less than 50,000 units, gordox – not less than 500,000 units in/in);
- antioxidant and antihypoxant therapy.
5
Detoxification:
- in severe acute pancreatitis, extracorporeal detoxification methods are indicated, of which the
most effective is serial therapeutic plasmapheresis (after BCC replenishment and in the absence
of endotoxin shock), followed by plasmosamination (1-3 sessions after 24-48 hours, the average
volume of plasmoexfusion is about 1 liter); each session of extracorporeal detoxification (in
addition to plasmapheresis) it should be accompanied by rehydration and correction of water-salt
metabolism in the mode of for ceddiuresis;
- the process of detoxification in severe acute pancreatitis can also be achieved by evacuation of
toxic exudates (peritoneal and retro-peritoneal) during laparoscopic (or laparocentesis), drainage
of the abdominal cavity and laparoscopic decompression of retroperitoneal tissue.
6
Antibiotic therapy (broad spectrum of action):
Cephalosporins of III-IV generations or fluoroquinolones of II-III generations in combination
with metronidazole.
 Jaundice is extremely serious problem in practice doctor. Jaundice is the yellow
coloration of the skin, sclera, and mucous membranes. shells, caused deposition bilirubin
due to excess its accumulation in blood. Yellowness of the skin and visible mucous shells
becomes noticeable when the level of serum bilirubin reaches 34 - 50 µmol/l, and distinct
at 120 µmol/l. Usually appears first yellow staining sclera, then - mucous shells, A later –
skin, latest turn yellow palms and soles. For identifying jaundice inspection the patient
should be carried out in daylight or when using daylamps
Allocate various shades icteric staining: lemon- yellow (characteristic for hemolytic
processes), orange red (characteristic of hepatocellular lesions), greenish (occurs with
prolonged subhepatic obturation), as well as dark olive, almost black (observed at very
lengthy cholestasis). Differential- the diagnostic value of these shades is relative, the
presence of one or other shade testifies first of all, O duration jaundice.
Not any yellow staining skin Can name jaundice. Exist other options yellow
staining skin, which not are "jaundice" in the medical sense of the word. These are the
so-called false jaundice. They also appear as yellow coloration of the skin or sclera, but not
conditioned elevated content bilirubin in serum blood.
From false jaundice allocate the following:
1. Deposition of fat on the conjunctiva at the corner of the eye, giving a slight yellowish
staining sclera, which never not combined with staining skin, always it happens on
limited plot. Sclera at this never all does not turn yellow bilirubin level in blood within
norms.
2. xanthomas, emerging in corner eyes. Simultaneously these yellowish education are
found on rear surfaces hands, often on extensor surfaces in areas elbow joint. Education
xanthoma observed at violation lipid exchange.
3. Icteric staining of the sclera and even the skin is possible when used inside some
medicinal drugs, for example akrikhin.
4. At renal insufficiency excess urochrome in blood maybe give yellow staining skin.
5. Peculiar yellow color skin maybe arise as a result excess carotene at use big quantities
carrots or pumpkins.
True jaundice is widespread syndrome at diseases liver, bile ways, a also lesions
systems erythropoiesis.
Before proceeding to the issues of differential diagnosis of jaundice, remember how
there is an exchange bilirubin.

Exchange bilirubin
Emergence jaundice always conditioned violation exchange bilirubin, formed as a
result of the breakdown of hemoglobin. It is known that hemoglobin consists of two main
parts - heme and globin. With hemolysis globin breaks up on aminoacids, a from gema in
cells RES - in bone bilirubin is formed in the brain, spleen and Kupffer cells. In general
difficulties formed per day from 100 before 300 mg bilirubin.
Main Part (near 80%) bilirubin formed behind check decaying erythrocytes (Fig. 1).
Rice. 1. General scheme metabolism bilirubin V body.
Behind day breaks up approximately 1% circulating in blood erythrocytes. At the
same time, the so-called shunt bilirubin is formed (it makes up 5 to 20%) of hemoglobin
decaying in the bone marrow erythroblasts, reticulocytes, as well as from some proteins,
containing heme (myoglobin, cytochromes, catalase, etc.). Bilirubin formed from heme
circulates with blood not soluble in water and transported albumin. It is called "indirect"
because it gives a positive van den reaction. Berg for bilirubin only with the addition of
alcohol or other reagents. At significant increase concentration indirect bilirubin in serum
blood (before 171-256 mmol/l) Part pigment not contacts with albumin. Indirect bilirubin,
not connected with albumin, is toxic for head brain.
With current blood indirect (free) bilirubin hits in liver
(rice. 2).
Rice. 2. Processes transformation free (indirect) bilirubin and mesobilinogen
(urobilinogen) in hepatic cell. bn - free (indirect) bilirubin; B-D -
bilirubin-glucuronide (connected, or straight bilirubin); M BG - mesobilinogen
(urobilinogen). Roman numbers indicate stages transformations.
1. I stage — capture bilirubin (B) hepatic cell after splitting off albumin;
2. Stage II - the formation of a water-soluble complex
of bilirubin- diglucuronide (B-D);
3. III stage — selection formed related (direct) bilirubin
(B-D) from hepatic cells in bile tubules (grooves).

At the vascular pole of the hepatocyte, bilirubin is separated from the carrier, i.e.
from albumin, and further moving through membrane hepatocyte with help special
transport enzyme, wearing name "ligandin", in microsomes, where contacts with
glucuronic acid. This reaction catalyzed enzyme UDP-glucuronyl transferase. Compound
bilirubin with glucuronic acid does his soluble in water. Formed conjugated (straight or
connected) bilirubin, which consists of mono- and diglucuronides, the latter makes up
75-80% of the excreted bile pigment. Direct bilirubin can pass through the renal filter, he
low toxicity for brain.
Connected bilirubin transported to biliary pole hepatocyte and stands out in
intestines due to active process under influence ATP. At human exists big reserve for
excretions bilirubin, so how healthy liver maybe highlight in a lot of once more bilirubin
than it is normally formed. At the same time, bilirubin excretion from hepatocyte - most
vulnerable link intrahepatic exchange bilirubin. In the extrahepatic bile ducts and in the
intestine from bilirubin urobilinogen is formed, part of which is absorbed through the
intestinal wall, hits v. Portae and is carried by the bloodstream to the liver (this is the
so-called enterohepatic circulation urobilinogen). Almost the whole this urobilinogen
captured hepatocytes and fully is destroyed. Only 1% of urobilinogen is not captured by
hepatocytes, but enters directly into the general blood flow and stands out in urine, where
under influence air and light is turning in urobilin.
The main amount formed in the bile ducts and intestines urobilinogen, undergoing
further transformation, stands out with feces in form stercobilinogen. Stercobilinogen in
straight gut and on light turns into stercobilin, which gives the feces a normal color. Small
part stercobilinogen, being sucked in lower departments thick guts by hemorrhoidal veins,
bypassing liver, hits in general blood flow and stands out kidneys. Normal urine always
contains footprints stercobilinogen, which is under action light goes into stercobilin.
Thus, the urine of a healthy person contains both stercobilin, and urobilin in trace
amounts. Urobilin and stercobilin are different chemical substances. Methods their
separation complex That's why at research their define together and designate like
urobilinoids.
Content bilirubin in serum blood healthy human is 6.8–20.5 µmol/l (according
to Yendrashik). Normal direct bilirubin is less ¼ general bilirubin in serum blood,
indirect bilirubin - rest ¾.

Classification jaundice
Despite on big quantity classifications jaundice, more often use their division into
suprahepatic, hepatic (intrahepatic) and subhepatic.
 Suprahepatic jaundice
Suprahepatic jaundice not connected with defeat liver, a conditioned excess
indirect (unconjugated) bilirubin in result increased destruction erythrocytes (pic. 3).

Pic. 3. The general scheme of bilirubin metabolism disorders in the body with
suprahepatic jaundice.
In these cases are primary lesions erythropoietic systems, significant decay
erythrocytes, what increases products gall pigment. It is known what liver capable
metabolize and allocate in bile quantity bilirubin, in 3-4 times exceeding normal
physiological level. If in blood rises level unconjugated bilirubin, means liver not manages
neither with transport of indirect bilirubin into microsomes, nor with conjugation process,
what testifies how minimum about 4 times promotion decay erythrocytes. It would seem
that, in this variant of jaundice, bilirubin should be always indirect because speech goes
about accumulation indirect free bilirubin. However, should consider, what in hepatic cage
arrives excess quantity bilirubin, he conjugated, and transport system breeding bilirubin
from cells maybe turn out to be insufficient, and then in the blood, along with indirect
bilirubin, the content whom will increased in first queue, simultaneously observed
increase in content and direct bilirubin.
We have dwelt in detail on the pathogenesis of this form of jaundice in order to
avoid an unnecessarily straightforward unambiguous approach to the assessment of direct
and indirect bilirubin. At suprahepatic jaundice content indirect (unconjugated) bilirubin
should prevail, it should be a lot of, but along with him maybe increase and direct
(conjugated) bilirubin.
 With the suprahepatic form of jaundice, another pathological process that seems to
be very important. Due to the excess of indirect bilirubin, the formation and excretion of
direct bilirubin into bile is possible, containing more than 25% monoglucuronide. Last
insoluble in water and maybe be the cause of education bile stones.
Patient’s faeces with suprahepatic jaundice has a darker color because of availability
in German elevated quantities stercobilinogen and stercobilin. In connections with
enlarged content bile pigments, falling in intestines, in general blood flow hits big quantity
urobilinogen, which cannot be metabolized in the liver. In connection with this urine rises
urobilinogen level .
Functional samples liver at this varieties jaundice usually substantially do not change.
suprahepatic (hemolytic) jaundice accompanied characteristic clinical triad: anemia,
jaundice, splenomegaly.
When examining patients hemolytic anemia in the peripheral blood determined
elevated quantity reticulocytes, and in bone marrow punctate - hyperplasia erythroid
sprout. Important laboratory sign hemolytic jaundice is shortening duration life
erythrocytes. In diagnostics use also such hematological research, how try Coombs (on
detection antibodies to erythrocyte antigen), electrophoretic study of hemoglobin types,
etc. With hemolytic jaundice, the serum level is significantly increased gland in serum
blood, comes to light hemoglobinemia and hemoglobinuria.
Hemolysis of erythrocytes can be intracellular and intravascular. At intracellular
hemolysis small quantity hemoglobin maybe hit in plasma, but here he straightaway same
contacts haptoglobin (α-glycoprotein) and again used for hematopoiesis.
At intravascular hemolysis hemoglobinemia sharp increases haptoglobin cannot
capture all of Hb and it appears in the urine - occurs hemoglobinuria. Urine sick It has at
this red, brown or almost black color.
The appearance of pathological hemolysis is associated with two main reasons:
change buildings erythrocytes (hereditary or purchased) or impact on normal erythrocytes
any external factors which cause hemolysis.
Allocate 2 groups hemolytic anemia - hereditary and purchased. Big part
hereditary hemolytic anemia accompanied cellular hemolysis.
IN group hereditary hemolytic anemia allocate anemia, related:
● With violation structures membranes erythrocytes - erythrocytopathy;
● With violation activity enzymes - fermentopathy;
● With presence genetic anomalies hemoglobin - hemoglobinopathies.
To erythrocytopathies applies hereditary microspherocytic anemia - disease
Minkowski-Choffard. Given disease conditioned hereditary defect in structure proteins
membranes erythrocytes, what leads to increased permeability of Na ions through the cell
membrane. Ions Na accumulate inside erythrocytes, which acquire form spherocytes, their
volume increases, and the diameter decreases, sharply decreases osmotic resistance, and
erythrocytes quickly destroyed in the spleen. This most widespread in middle and northern
lane Russia hemolytic anemia.
Disease it has usually family-hereditary character and transmitted in a dominant
manner. The literature describes the case when 9 members one and toy same families was
congenital hemolytic anemia with typical clinical signs: lemon yellow coloration skin and
mucous shells, splenomegaly, trophic ulcers shins, hemolytic crises. Father suffered
jaundice more 17 years and periodically, in connections with worsening states, acted in
hospital with diagnosis: "malaria". However malarial plasmodium in blood neither once
not found and antimalarial therapy effect not gave. Two his son 4 and 8 years and daughter
18 years died from jaundice. More one daughter behind 2 days before of death enrolled in
hospital in severe able with sharp pronounced anemia and perished in state of anemic
coma. Other 2 sons and 2 daughters suffer from jaundice throughout row years with
frequent crises, which accompanied promotion temperature, chills increased jaundice.
At disease Minkowski-Choffard duration life erythrocytes much shortened (before
7-14 days instead of 120 in norm). Clinical manifestations begin in children's age.
Sometimes only jaundice, in heavy cases hemolytic crises and symptoms anemia:
weakness, dizziness, heartbeat. Dermal covers lemon yellow coloring, in blood indirect
bilirubin, feces dark brown colors. Urine strong tea colors so how she has a lot of
urobilinogen.
Another sign of the disease is an enlargement of the spleen, it reaches large sizes
(1-2 kg). Patients often present with developmental anomalies (tower scull, saddle nose,
high standing solid sky) and trophic ulcers shins.
At disease Minkowski-Choffard content hemoglobin and quantity erythrocytes
lowered color index within norms. The main morphological sign of the disease is
microspherocytosis, i.e. availability in blood big quantities small round erythrocytes
(diameter reduced up to 5-6 microns). The Price-Jones curve is shifted to the left.
Erythrocytes are not changed only morphologically, they different also reduced osmotic
resistance.
Spherocytosis typical also and for autoimmune hemolytic anemia. In differential
diagnosis with acquired autoimmune hemolytic anemia should remember, what last, how
rule leaks heavier, how anemia Minkowski-Choffard. No instructions on family character
diseases, try Coombs positive missing anomalies development, osmotic stamina
erythrocytes lowered slightly, no microcytosis.
Of the group of fermentopathies, hemolytic is the most common. anemia, bound
with deficit activity enzyme glucose-6 phosphate dehydrogenase. At deficit this enzyme
violated aerobic oxidative path transformation glucose.
Some sick complain on permanent icterus sclera with children's years. Spleen
increased. At majority sick disease clinically not appears without special provocations
crises.
Hemolytic crises arise at admission quinine, sulfonamides, nitrofurans, 5-NOC, tubazid,
ftivazide, PASK, vicasola, aspirin and accompanied jaundice, fever highlighting urine black or
brown. Available indication on family character diseases. Diagnosis diseases tied with
definition activity glucose-6 phosphate dehydrogenase.
In our country from hemoglobinopathies more often occurs sickle-shaped cellular
anemia and thalassemia.
Sickle cell anemia is an inherited disorder that suffer children, inherited from
parents abnormal hemoglobin S. red blood cells sick acquire sickle-shaped shape. Except
anemia and jaundice in the clinical picture expressed symptoms associated with thrombosis
small vessels sickle-shaped erythrocytes.
Thalassemia. Disease conditioned congenital defect hemoglobin. Fetal hemoglobin
in a healthy person disappears from the blood after a few months after birth, in patients
with thalassemia, it persists for life. At heterozygous children who received a trait from
one of the parents are observed small and minimal forms thalassemia, which usually flow
without severe jaundice. Most patients homozygous for this pathology are dying in
childhood.
Diagnostic signs diseases: increased stability erythrocytes to hypotonic solution
chloride sodium, high content gland in serum blood, hypochromic anemia, characteristic
(target) form erythrocytes. Content in blood fetal hemoglobin in these patients sometimes
reaches 20%. Its content in a healthy a person is not exceeds 4%.
Acquired hemolytic anemia may be sharp and chronic and accompanied by
jaundice. It arises as a result autoimmune hemolysis, and when exposed to infections and
hemolytic poisons. Acute hemolytic anemia conditioned predominantly intravascular
hemolysis. Causes their varied:
● infections (sepsis, malaria and others);
● intoxication hemolytic poisons (phosphorus, snake, mushroom poisons, acetic acid
poisoning acid);
● physical factors (burns, cooling);
● transfusion incompatible blood;
● drugs: quinine, sulfonamides, some antibiotics.
Autoimmune hemolytic anemia meet most often among acquired anemias. With
these forms of anemia, the production of antibodies against antigen of own unchanged
erythrocytes. According to etiological principle autoimmune hemolytic anemia divide on
idiopathic (cause unknown) and symptomatic, when it is possible to establish the main
disease. More often total her turn out hemoblastosis, SLE, HAG, malaria, sepsis.
Disease starts sharply or subacute, among complete well-being appear weakness,
pain in lower back, heartbeat, fever, jaundice, which often accept behind OVG. At sick
comes to light splenomegaly. Main laboratory test, which indicates on immune character
hemolysis, is positive straight try Coombs. The aggregate-hemagglutination method is
even more sensitive.
Paroxysmal night hemoglobinuria (disease Markiafavy- Micheli) is acquired
hemolytic anemia with permanent intravascular hemolysis and highlighting with urine
hemosiderin. Hemolytic crises occur at night, are accompanied by pain in stomach and
thrombosis small veins. Pathognomonic for given diseases increased tendency of
erythrocytes to hemolysis when serum is acidified blood (Hine test).
To acquired hemolytic anemia refer hemolytic disease newborns, emerging at Rh
incompatibility blood mothers and fetus.
Hepatic jaundice
Hepatic jaundice conditioned violation intrahepatic exchange bilirubin (rice. 4, 5).
Rice. 4. Violation processes transformation bilirubin and mesobilinogen
(urobilinogen) in hepatic cage at hepatic jaundice.

Fig.5. The general scheme of violations of bilirubin metabolism in the body with
hepatic jaundice.
Known the following options violations various stages intrahepatic exchange
bilirubin:
● Impaired uptake of bilirubin by hepatocytes due to low levels ligandin. Like option
 jaundice It happens at fasting, after introduction of radiopaque substances inhibitory
ligandin.
● Violation of the process of conjugation of bilirubin with glucuronic acid in the result
of a decrease in the activity of uridine diphosphate-
glucuronyltransferase (UDF-GT). Violation processes conjugations maybe be
congenital and acquired. congenital violation processes conjugations observed at
syndromes Gilbert and Crigler-Najjar. At violation process conjugations rises level
free bilirubin and decreases content bilirubin in bile.
● Violation intrahepatic exchange bilirubin due to damage hepatocytes and their
cytolysis.
● Violation transport bile and in her composition direct bilirubin in bile capillary -
intrahepatic cholestasis. At the same time, it happens admission direct bilirubin from
hepatocyte straight in blood.
● Another variant of intrahepatic cholestasis is possible, in which transportation is
disrupted bile through the smallest bile ducts. This going on result compression bile
capillaries damaged edematous hepatocytes, which disrupts the evacuation of them
bile and creates conditions for increasing the resorption of direct bilirubin in blood.
Not last role here plays and defect transport enzymes. At intrahepatic cholestasis
selection bilirubin with bile into the intestines sharp decreases.
Exists some classifications hepatic jaundice in dependencies from level, on which
going on violation metabolism and transport bilirubin.
According to one from them, hepatic jaundice subdivide on hepatocellular and
posthepatocellular, A hepatocellular - additionally on premicrosomal, microsomal and
postmicrosomal .
In basis premicrosomal jaundice lie violation capture bilirubin by hepatocyte and
disruption of its connection with cytoplasmic proteins.
In the pathogenesis of microsomal jaundice, the leading role is played by a violation
conjugation of bilirubin with glucuronic acid, resulting in an increase in level unconjugated
bilirubin.
Postmicrosomal hepatocellular jaundice arises most often. At this option jaundice
violated excretion associated bilirubin in bile and going on admission his from hepatocyte
in blood, due to this in blood rises content conjugated bilirubin.
At posthepatocellular baked jaundice going on violation bile transport at the level of
intrahepatic ducts, resulting in conjugated bilirubin returns in blood.
In purposes detailing mechanisms, leading to development jaundice, A.I. Khazanov
offers next classification hepatic jaundice:
● parenchymal-microsomal;
● parenchymal-cytolytic;
● parenchymal excretion;
● parenchymal-cholestatic;
● canalicular-cholestatic.
 Represented classification hepatic jaundice close between themselves and
complement each other. In classification A.I. Khazanova not reflected violation
premicrosomal metabolic stage and bilirubin transport, but in her found reflection very
important mechanism development hepatic jaundice - cytolysis hepatocytes
(parenchymal-cytolytic jaundice). Besides, A.I. Khazanov highlights parenchymal
excretion jaundice (syndrome Dubin-Johnson and syndrome Rotor), emphasizing her
difference from parenchymal - cholestatic jaundice. Parenchymal-cholestatic jaundice
correspond postmicrosomal hepatocellular jaundice, a canalicular-cholestatic -
post-hepatocellular.
At further presentation material will used both classification.
It should be borne in mind that several phases of intrahepatic bilirubin metabolism may
be disrupted in the same patient, while violation of one of the phases prevails.
PARENCHYMATOUS-MICROSOMAL JAUNDICE
conditioned insufficiency enzymes responsible behind conjugation bilirubin with
glucuronic acid and is characterized by accumulation in the blood unconjugated bilirubin
Accumulation in blood unconjugated bilirubin is seen in hereditary non-hemolytic
jaundices, among which are currently distinguish syndrome Gilbert and Crigler-Najjar.
SYNDROME GILBERT in all cases wears hereditary character and is transmitted
in an autosomal dominant manner. More than half cases clinically first appears in
connections with sharp diseases (more often total in running out acute hepatitis A). Then
conditionally they say about "post-hepatitis" form syndrome Gilbert, meaning at this, what
viral hepatitis plays role factor a, revealing hereditary defect.
Etiology and pathogenesis. At syndrome Gilbert is genetically conditioned failure
in hepatocytes enzyme UDF- glucuronyltransferase, with help whom carried out
conjugation bilirubin with glucuronic acid. Becides, going on violation transport functions
proteins, delivering unconjugated bilirubin to the endoplasmic
hepatocyte network.
Gilbert's syndrome, as a rule, is observed at a young age. At 90% cases disease
manifests in 20-30 year old age. Much more often meets at men (10:1) by comparison with
women. In general syndrome Gilbert meets at 1-5 % population.
Clinic. In clinical picture diseases leading symptom is chronic or intermittent
jaundice. Its degree fluctuates wide limits: from subicteric sclera before pronounced
jaundice skin. Color urine not changed, maybe brightening feces. Often jaundice the only
one symptom and comes to light at survey sick by about others diseases.
Yellowness of the sclera and skin is first detected in childhood and usually
intermittent. Exacerbations can be provoked mental or physical overvoltage, reception
alcohol, errors in diet, reception drugs, infection in bile ways.
Sick worries pain or feeling gravity in law hypochondrium, dyspeptic disorders.
Possible complaints asthenic character.
Hepatomegaly observed at 25-60% sick, although and expressed slightly. At
majority sick liver on 1-2 cm speaks from under costal arcs by mid-clavicular line,
consistency her soft, palpation painless.
For Gilbert's syndrome typical isolated character indirect hyperbilirubinemia, which
only at individual sick exceeds 50-70 µmol/l. All rest functional hepatic samples, and also
serological indicators normal. At syndrome Gilbert bilirubinuria is absent, the number of
urobilin bodies in feces and urine, as rule not changed.
Transient moderate promotion activity AlAT, ASAT, LDG-5, moderate
dysproteinemia not contradict diagnosis syndrome Gilbert. Indicators functional samples
liver topics more often there are changed how longer term diseases.
Flow syndrome Gilbert in overwhelming most cases wavy, with periodical
exacerbations.
One from most convincing diagnostic samples at syndrome Gilbert is try with
introduction inductors transport proteins and glucuronyltransferase - phenobarbital or
zixorin. 10 days after start reception phenobarbital by 0.05 G 2-3 times in day or through
5-7 days taking zixorin 200 mg 3 times a day, patients have a significant decline or
normalization bilirubin level.
Treatment. In connection with a favorable prognosis in all respects, a person with
syndrome Gilbert need only in staging precise diagnosis, treatment phenobarbital or
zixorin in specified doses in flow 2-4 weeks intensive psychotherapy, which, how rule
leads to relief well-being sick.
SYNDROME KRIGLER NAYYAR It has hereditary nature, transmitted by
autosomal recessive type.
Etiology and pathogenesis. Pathogenetic the basis syndrome - absence in
hepatocytes of glucuronyltransferase and, therefore, a complete inability liver conjugate
bilirubin.

Duration life erythrocytes, that there is products bilirubin, not broken, and the main
way of removing the pigment from the body is blocked. In connections with this in blood
installed constantly high level unconjugated bilirubin, which is toxic to CNS, causing
development so called nuclear jaundice.

Clinic. The clinical manifestations of the disease consist of pronounced jaundice

and heavy neurological violations. Jaundice appears straightaway same after birth and
preserved in flow all life. Get sick equally often and boys, and girls. Chair aholic, in bile
discover only footprints bilirubin. Liver at some sick increased in sizes. Symptoms defeat
CNS appear in breastfeeding age and expressed in convulsions opisthotonus, nystagmus.
Sick children lagging behind in mental and physical development.

Indicators free bilirubin in serum blood reach 324-528 µmol/l, those. Higher norms in
15 -20 once. Encephalopathy takes in clinical picture dominant place. Sick perish in
early children's age
PARENCHYMATUS-CYTOLYTIC JAUNDICE. Leading meaning in pathogenesis it
has violation permeability and integrity membranes of hepatocytes with the release of
direct bilirubin into the bloodstream. This view jaundice it has place at acute and chronic
damage liver (hepatitis and cirrhosis) and appears in form characteristic changes pigment
metabolism. Increased blood levels of both direct and indirect bilirubin, comes to light
bilirubinuria. Partially bilirubin arrives in bile, so there is stercobilin in the feces. The level
of urobilin in the urine is increased due to the fact that it is not captured by damaged
 hepatocytes.
At parenchymal-cytolytic jaundice there are clinical and laboratory signs defeat
liver. Reflection syndrome cytolysis is an increase in serum activity of aminotransferases:
ALT and ASAT. In last thing time use parallel definition activity AlAT in whole and
divorced serum blood. This connected with topics what aminotransferase, having hit from
cytolysis serum blood, form polymer complexes in which the active centers are closed,
and when the serum is diluted, they open. In patients with AVH, ALT activity significantly
higher in diluted whey than in whole whey. HCV is not typical.
In differential diagnostics it has meaning grade ratios enzymes. So, ratio
ASAT/ALAT = 2 characteristically for alcoholic defeat liver, and ASAT/ALAT = in1 - for
hepatitis A, intrahepatic cholestasis. In liver cirrhosis, liver metastases, AST activity is
higher, how AlAT.
With damage to the mitochondria of hepatocytes, there is an increase in the blood
LDH activity. This is especially typical of alcoholic liver damage, so how alcohol
metabolized in mitochondria. Moderate promotion LDH at significant increase activity
ASAT and AlAT is typical for hepatic (parenchymal) jaundice. Significant (in 8-10 once)
increase activity LDH at moderate activity ASAT and AlAT characteristically for
subhepatic jaundice. So the way attitude ASAT/ALAT gives opportunity differentiate viral
and alcoholic defeat liver, and attitude LDH/AlAT - performance about inside- and
extrahepatic cholestasis.
Raise general activity LDH maybe be observed at many diseases liver and others
organs. In differential diagnostics the ratio of LDH isoenzymes is essential. For defeat
hepatocytes are characterized by an increase in LDH-5 activity. Long Magnification
activity LDH-4 And LDH-5 gives grounds suspect metastases in liver.
At parenchymal-cytolytic jaundice, how rule there are manifestations of the
syndrome of hepatocellular insufficiency: hypoalbuminemia, decline level prothrombin,
factors V, VII, IX, X, fibrinogen, which may contribute to the development of hemorrhagic
syndrome. violated interstitial exchange proteins, fat and carbohydrates and weakened
protective function liver.
Clinic. Icteric coloration skin, extrahepatic signs, increase liver, often increase
spleen, signs hepatocellular insufficiency, possible symptoms portal hypertension.
PARENCHYMATIC-CHOLESTATIC JAUNDICE
(intracellular cholestasis) most often observed at acute medicinal hepatitis (at admission
chlorpromazine, anabolic steroids androgens, sulfonamides) and cholestatic form viral
hepatitis A.
In basis parenchymal-cholestatic jaundice lies violation mechanisms of formation
and transport of bile at the level of hepatocyte and excretion it from the hepatocyte into the
bile ducts (intracellular cholestasis). This type jaundice is characterized by an increase in
serum levels of total bilirubin with predominance conjugated (direct). Selection urobilin
with urine and stercobilin with feces lowered or absent. Revealed characteristic clinical
and biochemical symptom complex: itching skin, promotion activity enzymes cholestasis,
bile acids, cholesterol.
CANALICULAR-CHOLESTATIC JAUNDICE arises in as a result of violation of
the outflow of bile through the intrahepatic biliary tract and characterized direct
 hyperbilirubinemia. Seen in primary biliary cirrhosis, sclerosing cholangitis,
cholestatic hepatitis.
PARENCHYMATO-EXCRETIONAL JAUNDICE. To her
include Dubin-Johnson and Rotor syndromes. Some authors include these diseases in the
group of hepatic cholestatic jaundices, others with similar interpretation these diseases Not
agree because the at them only partially violated excretory hepatocyte function.
SYNDROME DABIN-JOHNSON. Disease It has hereditary nature, transmitted
over autosomal dominant type.
Pathogenesis. Violated selection from hepatocyte bilirubin, cholecystographic
funds, bromsulfalein, Bengali pink, but violation excretions Not distributed by on bile
acids. Consequence this is deviation from norms indicators bilirubin, bromsulfalein test, as
well as the frequent absence of a shadow of the gallbladder at cholecystography.
Usually content general bilirubin reaches 68 –138 µmol/l.
Determined only straight bilirubin or prevails his fraction.
Due to violations excretory functions hepatocyte in German accumulates pigment
(nature his not known), imparting liver unusual color - from greenish gray to brown-black.
Clinic. The first clinical manifestations may appear during with birth up to 40 years
old age. Disease more often meets at men.
Basic syndrome - chronic or intermittent jaundice, unsharp expressed. At majority
sick celebrated moderate liver enlargement, light feces and dark urine are periodically
observed. At a third of patients have no subjective manifestations. In the rest of the patients
there are complaints, characteristic of astheno-neurotic syndrome.
Syndrome Dubin-Johnson Can distinguish from others forms hyperbilirubinemia by
increasing the concentration of bromsulfalein in the blood 2 hours after the start of the
study and lengthening the elimination half-life bengali pink, labeled I 131 , before 7 hours.
ROTOR SYNDROME. The pathogenesis of Rotor syndrome is similar to that at
syndrome Dabin-Johnson, But at syndrome Rotor defect excretions less pronounced.
Therefore, in the presence of many similar clinical signs and violations pigmented
exchange missing characteristic violations excretory function during the bromsulfalein test,
oral cholecystography gives positive result.
Macroscopically liver usually not changed in hepatocytes not contained unidentified
pigment, characteristic for syndrome Dubin-Johnson.
Disease equally often strikes men and women. First clinical manifestations possible
already in children's age. Basic clinical symptom is mild jaundice. In some patients, the
liver somewhat enlarged. Darkening of urine is observed periodically. The course of the
Rotor syndrome is favorable, the disease lasts for many years. By- apparently changes,
ongoing at syndrome rotor, not affect on duration life.
Treatment. Treatment of patients with Dubin-Johnson and Rotor syndromes is not
developed, but common are recommendations avoid physical and emotional overload,
reception alcohol, stick to regime nutrition.
Once again, we emphasize that hepatic jaundice can occur with unconjugated,
so and with conjugated bilirubin.
 HEPATIC JAUNDICE WITH UNCONJUGATED
BILIRUBIN is caused by a violation of the uptake of bilirubin by the hepatocyte,
processes by combining it with cytoplasmic proteins, transport to microsomes and
conjugations with glucuronic acid.
HEPATIC JAUNDICE WITH CONJUGATED
BILIRUBIN arises V result:

1) direct defeat hepatic fabrics (cytolysis hepatocytes):

● agents infectious-parasitic origin (viruses, bacteria and their toxins);
● toxic factors (organic poisoning and inorganic poisons,
high doses alcohol);
● hepatotropic AT And sensitized lymphocytes;
● tumor process.
2) Intrahepatic cholestasis (impaired excretion of bile from hepatocytes
and transport bile by intrahepatic ducts);
Intrahepatic cholestasis
Hepatic jaundice with conjugated bilirubin maybe be conditioned intrahepatic
cholestasis, which characterized decrease receipts bile in 12 duodenal intestine at absence
obstruction extrahepatic biliary tract. Intrahepatic cholestasis can develop at the level of
the hepatocyte, which is observed in parenchymal cholestatic jaundice and/or on level
intrahepatic bile ducts in canalicular-cholestatic jaundice.
Cholestasis ON LEVEL HEPATOCYTE Maybe be conditioned viral, alcoholic,
medicinal, toxic defeats liver, stagnant cardiac insufficiency, metabolic violations (benign
returnable intrahepatic cholestasis, cholestasis pregnant women cystic fibrosis, α 1
-antitrypsin failure and etc.). With this form, the excretion of bile in the zone of the biliary
pole is disturbed. hepatocyte due to defeat enzymatic systems, responsible behind
excretion bile.
Cholestasis at the level of intrahepatic biliary
PROTOKOV It has place at primary biliary cirrhosis liver, primary and secondary
sclerosing cholangitis and etc.
At cholestasis excess concentration components bile causes row hepatic and
systemic defeats. Main role belongs detergent action bile acids.
The clinical manifestations of cholestasis are fairly similar, regardless of etiology
and mechanisms of its development. They are based on three factor a:
● excess admission elements bile in blood;
● decrease quantities or absence bile in intestines;
● impact components bile on hepatic cells and tubules.
For intrahepatic cholestasis, except jaundice, characteristic such symptoms, how
cutaneous itch, xanthomas, xanthelasma, dark urine, and also systemic manifestations:
acute renal failure, development of acute ulcers and erosions in the stomach, bleeding. Bile
deficiency in the intestine is accompanied by steatorrhea, syndrome malabsorption, deficit
fat soluble vitamins, violation mineralization bones. excess quantity components bile in
hepatocytes and canaliculi leads to their necrosis and development of hepatocellular
insufficiency. If cholestasis does not resolve, that through 3-5 years formed cirrhosis liver.
severity and expressiveness clinical symptoms at intrahepatic cholestasis extremely
variable and often cholestasis leaks asymptomatically (for example, drug), when his the
only manifestation is violation biochemical samples liver.
laboratory diagnostics cholestasis based on definition in blood alkaline
phosphatases, GGTP, general bilirubin and his factions, cholesterol aminotransferases.
Subhepatic jaundice
Subhepatic jaundice is yourself persistent violation breeding bile from bile ducts and
gall bubble in clearance 12- duodenal intestines. In table 1 main etiological factors
subhepatic jaundice.
Table 1
Etiological factors subhepatic jaundice
Subhepatic
Malignant genesis benign genesis
- cancer heads pancreatic glands - choledocholithiasis
- cancer obd - spicy and chronic pancreatitis
- cancer gall bubble - cicatricial stricture choledochus
- cancer bile ducts - stenosis obd
- metastases V gates liver - pericholedochial lymphadenitis
- sclerosing cholangitis

Violation of the outflow of bile leads to its stagnation (cholestasis), increased

pressure in bile capillaries, their overstretching, raising wall permeability and rupture,
which contributes to the flow of bile into the blood how directly, so and through lymphatic
way. Appearance bile in blood leads to development cholemic syndrome, which appears
severe pruritus and bradycardia. With complete obstruction of the bile ways and
termination receipts bile in guts feces becomes acholic, those. discolored it has clayey,
white-grey color.
For subhepatic jaundice characteristically following violation pigment
metabolism:
● promotion in blood general and especially direct bilirubin;
● the appearance of bilirubin in the urine, which causes dark staining;
● lack of urobilinogen in the urine with complete blockage biliary ducts;
● absence or downgrade stercobilinogen in faeces (rice. 6).
Rice. 6. General scheme of bilirubin metabolism disorders in the body with
subhepatic jaundice.
One from major clinical manifestations subhepatic jaundice (extrahepatic
cholestasis) is cutaneous itching. At carrying out differential diagnosis between
intrahepatic and extrahepatic cholestasis, it should be remembered that intrahepatic
cholestasis is characterized by relatively early appearance itching. Itching preceded others
manifestations diseases. Maybe be observed dumb, pulling pain in areas liver. Revealed
increase liver and sometimes splenomegaly. For subhepatic jaundice against the
background of cholelithiasis is characterized by the presence of intense, spastic pain.
Itching appears later.
For cholestatic syndrome (intrahepatic and subhepatic) typical is an increase in the
activity in the blood serum of a number of enzymes: alkaline phosphatases,
γ-glutamyltransferases, 5-nucleotidase. At carrying out differential diagnosis should have
in mind what at extrahepatic obstruction, alkaline phosphatase activity increases 10 times
or more, while time how intrahepatic cholestasis usually accompanied promotion activity
AP at 2-3 times.
To characteristic manifestations cholestasis refer also violations lipid exchange. Due
to violations synthesis and excretions cholesterol hypercholesterolemia occurs, the
coefficient increases cholesterol/phospholipids. Clinical manifestation of
hypercholesterolemia in long cholestasis is his deposition in skin, especially on centuries
(xanthoma, xanthelasma). Cholestasis is accompanied by a significant increase content
β-lipoproteins and decline α-lipoproteins in serum blood.
With cholestasis, there is an increase in the content of free fatty acids, mainly due to
saturated ones, with a slight decrease unsaturated increase in fatty acids in composition
triglycerides.
Mechanism violations fatty exchange at cholestasis explain in the following way.
When blocking the flow of bile into the intestine, changes enterohepatic circulation bile
acids, incoming in liver from gate veins. coming at this decline concentration secondary
bile acids is a factor that stimulates the activation of the synthesis cholesterol, bile acids
and membrane-dependent enzymes (ALP, GGT, 5-nucleotidase). It has meaning also
difficulty receipts cholesterol in bile capillaries in connections with bile hypertension.
How for intrahepatic, so and for extrahepatic cholestasis characteristic is decline
level prothrombin in serum blood. In result blockade receipts bile in intestines going down
suction fat and dissolving in them vitamins, in volume including vitamin K to necessary for
education prothrombin. Hypoprothrombinemia maybe be also consequence violations
functions liver at parenchymal cytolytic jaundice. Differentiate these states allows try
Koller. So, in answer on introduction vitamin K to at cholestasis distinctly rises level
prothrombin, and at parenchymal-cytological jaundice significant changes not comes.
In the differential diagnosis of intrahepatic and extrahepatic cholestasis, a number of
instrumental methods are used to identify localization and reason obstruction biliary tract.
Most informative retrograde pancreatocholangiography and percutaneous cholangiography.
However for productions diagnosis have also meaning laparoscopy with sighting biopsy
ultrasonic study, computed tomography of the biliary tract and duodenoscopy (examination
of a large duodenal papilla intestines).
If subhepatic jaundice is diagnosed, that necessary to figure out her reason.
Blockage of the bile ducts is most commonly caused by either stone or tumor.
Let's try differentiate these two fundamentally various states.
Choledocholithiasis - most frequent cause subhepatic jaundice. Let's clarify details,
characteristic for jaundice, caused choledocholithiasis and tumor. Jaundice, conditioned
blockage stone general gall the duct, as a rule, appears after severe pain, i.e. initially
bilious colic, then jaundice. With obstruction of the bile ducts by a stone, jaundice arises
enough fast - in flow days. Jaundice on soil tumors develops slowly and, how rule her
emergence not preceded painful attack.
Pain at jaundice, caused a tumor usually are localized not in law hypochondrium,
and in epigastric areas or in central areas belly. For jaundice on background
choledocholithiasis characteristically promotion body temperature, as bile stasis leads to
cholangitis. With jaundice, related with a tumor temperature body maybe or stay normal or
be elevated, or even wear character "wicked", high and very remind hectic. At complete
obturation gall duct her must be eliminated within 3-5 days, otherwise acute hepatic
failure, from which sick, how rule not come out.
More often, obturation of the bile ducts with a stone is incomplete. In this case
jaundice is undulating. Serum bilirubin level although and reaches high values, but rarely
surpasses 170 mmol/l. At sick with such form jaundice itching absent or he not so sharp
expressed how at cholestatic hepatitis. In that same time at tumors jaundice constant, is
growing itch, ahead of herself jaundice. At stone bilious bubble, how rule fast wrinkled,
and at jaundice, related with tumor, the gallbladder is usually enlarged (Courvoisier-Terrier
symptom). Liver at jaundice, conditioned stone maybe be increased or not changed. At
tumors, flowing with jaundice, very often liver already amazed metastases, that's why she
much increased and, becides, dense and bumpy. The spleen in cholelithiasis is not
enlarged, with tumors often it happens increased. Constant satellite subhepatic jaundice
- an increase in the activity of alkaline phosphatase, but with a stone, the increase in the
activity of alkaline phosphatase is less than at tumors. And last syndrome — ascites,
which, how rule accompanies jaundice conditioned a tumor and absent at cholelithiasis
illness.
Hepatic duct stones tend to cause the same clinical picture that common bile duct
stones. The bile duct stones are not lead to jaundice but they call dropsy of the gallbladder.
Jaundice occurs in volume case, If stone wedged in general bilious duct. Stones big
duodenal papilla especially often accompanied complete obturation biliary tract and rack
mechanical jaundice.
Cause subhepatic jaundice may be cicatricial strictures extrahepatic bile ducts.
They arise after operations.
Not less important differential diagnostics jaundice, caused tumor various
localization. More often total jaundice conditioned cancer pancreatic glands.
Characteristic expressed painful syndrome; localization - the epigastric region, less often -
the left hypochondrium, girdle pain. The gallbladder is usually enlarged in pancreatic
cancer. (positive Courvoisier-Terrier sign), glucosuria and hyperglycemia, falls content
pancreatic enzymes. At X-ray research in 12 duodenal gut is found indirect sign tumors
heads pancreatic glands – straightening "horseshoe" of the duodenum due to an increase in
the head of the pancreas glands.
Pretty early, a pancreatic tumor metastasizes to the liver, which increases and
becomes bumpy. Big help in diagnostics is ultrasound. Ultrasound allows early and reliably
diagnose tumor pancreatic glands.
Other localization tumors — big nipple duodenal intestines. This localization of
the tumor is characterized by the fact that the disease develops little by little often without
pain or pain moderate intensity. Often is found increased bilious bubble, positive symptom
Courvoisier. Characteristic complete obstruction with negative reaction on bile pigments in
urine and faeces and stable bilirubinemia before 500 µmol/l and combination jaundice with
bleeding and black feces. Diagnosis put with help duodenoscopy, radiologically can
discover filling defect 12 duodenal intestines.
Jaundice maybe be observed at lymphogranulomatosis, at his abdominal form in
result compression general gall duct lymph nodes. For Hodgkin's disease characteristic
typical clinical painting. The most common symptoms are enlarged lymphatic nodes and
spleen, leukocytosis and lymphopenia, increased ESR. Accurate diagnosis put at biopsy
lymph node.
And more one option tumors — hypernephroma right kidneys. Hypernephroma
with right sides maybe be accompanied sprouting in liver and call jaundice. For most
hypernephromas characteristic constant hematuria, possible leukocyturia. Pain sensations
are inconsistent. Main diagnostic triad hypernephromas: hematuria, pain, enlarged bud,
which can define at palpation.
Diagnostic program at hepatic and subhepatic jaundice
Consists of 2 stages of diagnostics. First set the character jaundice, and
then, if it is subhepatic jaundice, determine reason and localization obturation.
At stage 1, the diagnosis is based on clinical and biochemical research
(tab. 2)
Table 2
Main laboratory signs jaundice various origin

Laboratory signs Kinds jaundice

Parenchymal Mechanical Hemolytic
Bilirubin V blood Direct and Straight promoted Indirect
indirect promoted
raised
Bilirubin V urine Available Available Absent
Urobilin V urine Available Absent Available

(mesobilinogen) (stercobilinogen)
Sterkobilin V kale Available, Absent Available
but May be
lowered
 Ultrasound plays big role in differential diagnostics hepatic and subhepatic
jaundice and must be carried out first from instrumental methods research.
The diagnostic capabilities of the ultrasound method allow define:
● character jaundice: parenchymal or mechanical;
● make a differential diagnosis between jaundice benign and tumor genesis;
● establish the level of obturation of the bile ducts in case mechanical nature.
Diagnostic possibilities method have certain limits, however do not reduce the value
of the method.
Diagnostics jaundice parenchymal character with help ultrasonic method research
not is special difficulties. To her may drive spicy hepatitis, ultrasonic painting whom
characterized increase liver, decline echogenicity liver, promotion pericholedochal
echogenicity behind check serous edema perivascular fiber. At cirrhosis liver noted diffuse
heterogeneity liver, availability multiple obliterated vessels, an increase in the left lobe
with atrophy of the right, rounding of the corners of the liver, signs portal hypertension.
Main echographic sign parenchymal character jaundice is the presence of undilated
intra- and extrahepatic bile ducts.
Key sign mechanical jaundice at ultrasound is extension bile ducts (pic. 7), how
extrahepatic so and intrahepatic. In norm intrahepatic bile ducts, behind with the exception
of equity shares, which can be inspected only in 50% of cases, with ultrasound not visible.
Degree extensions bile ducts at mechanical jaundice depends on the causes of violation of
the outflow of bile and, to a greater extent, on duration obstruction. Dilatation intrahepatic
ducts maybe reveal on 3-5 day after obstruction. Extension ducts in series distributed by
from places blockages from below up. Intrahepatic dilated ducts in this case look like
saccular or tubular structures and in difference from branches gate veins save significant
degree extensions and traced practically before periphery. Difficulties in identifying dilated

intrahepatic ducts arise in volume case, when mechanical jaundice arises sharply and by
time is short, in case transient cholestasis at valve stones, at small stones choledochus,
which cause short-term violation patency.
Most frequent cause mechanical jaundice is choledocholithiasis (fig. 8). Diagnosis reliable
in case definitions in lumen choledochus hyperechoic structures with acoustic shadow. On
basis this ultrasonic sign stones are detected only in 30-35% of cases. Relatively low
percentage of detection of stones in the lumen of the duct with ultrasound is explained by
the fact that in most cases obstruction is caused by stones, located in the distal
choledochus, visualization of which is difficult due to retroduodenal location.
At availability strictures hepaticocholedochus in zone narrowing rendered in the form of a
narrow, sharply deformed tube. The walls of the duct on a significant stretch sharply
thickened due to expressed sclerosis.
Diagnostics mechanical jaundice, caused squeezing distal department choledochus
head pancreatic glands due to acute and chronic pancreatitis, enough high. This
conditioned good visualization at ultrasound pancreatic glands and opportunity with help
method estimate her state. Sonographic painting characterized increase heads pancreatic
gland, heterogeneity structures, fuzziness contours, decline echogenicity.

With tumor genesis of obstruction (Fig. 9) of the distal choledochus determined

sharp extension inside — and extrahepatic ducts and pronounced enlargement of the
gallbladder, which is explained by prolonged stagnation bile. At the same time, the
expansion of the Wirsung duct is observed in 9% cases at tumors distal department
choledochus, in 40 % at tumors heads pancreatic gland, in 67% at tumors BDS. By
availability strictures hepaticocholedochus in zone narrowing rendered in the form of a
narrow, sharply deformed tube. The walls of the duct on a significant stretch sharply
thickened due to expressed sclerosis.
Diagnostics mechanical jaundice, caused squeezing distal department choledochus
head pancreatic glands due to acute and chronic pancreatitis, enough high. This
conditioned good visualization at ultrasound pancreatic glands and opportunity with help
method estimate her state. Sonographic painting characterized increase heads pancreatic
gland, heterogeneity structures, fuzziness contours, decline echogenicity.
With tumor genesis of obstruction (Fig. 9) of the distal choledochus determined
sharp extension inside — and extrahepatic ducts and pronounced enlargement of the
gallbladder, which is explained by prolonged stagnation bile. At the same time, the
expansion of the Wirsung duct is observed in 9% cases at tumors distal department
choledochus, in 40 % at tumors heads pancreatic gland, in 67% at tumors BDS.
Pathognomonic complex for tumors heads pancreatic gland is a combination of a
direct symptom: local enlargement of the head behind check availability tumor-like
education various echogenicity, but predominantly reduced with indirect, to which relate:
ectasia chief pancreatic duct, phenomena chronic pancreatitis, arising from the blockade of
the duct by the tumor, as well as the expansion of intra- and extrahepatic ducts, increase
gall bubble.
Most difficult for ultrasound diagnostics is pathology BDS.
Ultrasonic diagnostics tumors obd based on indirect symptoms because the visualize
this education in form tumor masses of different levels of echogenicity in the OBD zone
are rarely possible. Indirect a sign of cancer is cholangioectasia throughout the biliary tree,
at blockade mouth Virsungova duct — pancreatectasia. Tumors obd and tumors outgoing
from distal parts choledochus, have similar echographic picture and practically not
distinguishable between yourself.
Tumors medium departments choledochus give at ultrasound picture, reminiscent at
tumors heads pancreatic glands. Difference is in volume, what tumors choledochus less
often visualized because of the predominance of infiltrative growth, and most often they
germinate cystic duct. Diagnostics tumor germination cystic duct is based on the definition
of a specific picture of the gallbladder, when his increase accompanied promotion
echogenicity internal contents, which is typical for a long-term disconnected gallbladder
from extrahepatic bile ducts.
Tumors extrahepatic bile ducts have more often increased echogenicity. important
indirect sign, which observed in 100% cases is cholangioectasia. Exception may make up
sick, at which jaundice absent in connections with overlay previously bilidigistive
anastomoses. For tumor occlusion equity duct characteristic intrahepatic cholangioectasia
on side defeat. At localization cancer in zone gate liver and proximal department hepatic
duct cholangioectasia determined in both shares liver. General hepatic bile duct below
tumors and bilious bubble in this case sleeping.
Cancer gall bubble is difficult diagnosed tumor. Difficulties diagnostics conditioned
topics what tumor develops on background for a long time existing cholelithiasis, structure
her is different more often elevated echogenicity. The main feature is the visualization of
the tumor mass, having intra- or extraorganic height. At blockade tumor
hepaticocholedochus develops cholangioectasia higher tumors.
Thus, ultrasound provides important information in organ diseases.
hepatopancreatoduodenal zones, complicated mechanical jaundice. Practical advantage
method is in volume, what ultrasound allows cut diagnostic period, data ultrasound can use
for building programs diagnostic research. However diagnostic capabilities of the method
have a limit of accuracy, so the data ultrasound needed verify others methods research.
At instructions on diffuse defeat liver and unchanged bile ducts most probable hepatic
jaundice, causes which may be deciphered with help immunological and morphological
research.
In the absence of significant reasons explaining jaundice, following ultrasound carry
out esophagogastroduodenoscopy. With her help determined pathology upper departments
gastrointestinal tract: varicose veins of the esophagus, tumors of the stomach, major
duodenal papilla, stomach deformity and 12 duodenal guts due to crushing her from the
outside.
If duodenoscopy does not reveal a defect, it should be carried out endoscopic
retrograde cholangiopancreatography, allowing estimate bile ducts and pancreatic ducts
glands.
If there is reasonable suspicion of pancreatic cancer carry out selective angiography.
Most clear angiographic indicators determined at tumors hepatopancreatobiliary systems.
At failed ERCP Maybe be carried out percutaneous hepatocholangiography.
Laparoscopy apply in those cases, when listed events not led to certain diagnosis.
Laparoscopy at jaundice allows specify localization pathological hearth. special value this
method acquires in those cases, when he combined with laparoscopic
cholecystocholangiography, allowing already in preoperative period get full intelligence
about character jaundice, level obstruction bile ducts and their anatomical and functional
condition. In hepatitis, the liver usually has a red-brown tint, and at for a long time current
disease becomes greenish grey. Biliary the bladder in all cases is collapsed and has a
sluggish tone. At obstructive jaundice visual picture depends on the level of obstruction
and duration of cholestasis. In the early stages of cholestasis, the liver has a reddish shade,
in some places on its surface greenish areas are determined. At prolonged cholestasis, the
liver becomes a dense consistency, enlarged in sizes, tense, with a pronounced greenish
tint. Most sick enlarged, tense bilious bubble.
In complex contemporary funds diagnostics and differential diagnostics jaundice
important meaning have radioisotope methods research. They make it possible to
determine the position, size, shape liver, its absorption-excretory function, state gall bubble
and patency biliary ducts. Most often with this purpose apply colloidal solutions
radioactive gold I96 Au, Bengal pink, labeled 131I, and short lived radionucleotide
technetium 99 Te. Choice drug for research depends from delivered clinical goals.
To detect hepatocellular changes in the liver or disorders outflow bile in intestines
applied Bengal pink, labeled 131I , which from blood captured polygonal cells and output
with bile in bile ducts and intestines without repeated suction in intestinal tract. At
obstructive forms cholestasis at majority sick determined moderately expressed violation
absorption and sharp pronounced violation of the excretory function of the liver. With
parenchymal forms jaundice violated how absorption, so and excretory function liver,
amplitude hepatograms it happens low excretory segment pronounced weakly and often
absent.
Colloidal solutions radioisotope gold 196 AI are captured reticuloendothelial cells
liver, held in them in flow several days and allow get clear images body on scanogram. In
liver tumors, the scanographic picture is characterized by moderate increase sizes liver and
violation contrast ratio in individual plots body, i. e. appearance defects accumulation
isotope. icteric forms hepatitis a most often appear in uniform increase liver with
homogeneous some reduced distribution isotope. In biliary cirrhosis, there is usually a
deformity of the liver with an increase in one of the shares and a decrease in the other, a
decrease in accumulation drug in regional departments on the border between the right and
left lobes of the liver a nd increase drug accumulation in
spleen.
In a study with radioactive technetium ( 99 Te), it is possible to evaluate not only
functional state liver, but and define clear visualization inside- and extrahepatic bile ducts
and gall bubble.
In last thing time big meaning attached research hepatopancreatobiliary systems
with help computer tomography.
 All listed methods at one sick in complete volume, how rule not apply. More often
total after holding several species research diagnosis becomes clear and need in further
research disappears.

Instrumental methods, used at survey sick with jaundice

1. Ultrasound of the liver, gallbladder, bile ducts (intra- and
extrahepatic), pancreatic gland, spleen, gate veins.
2. Esophagogastroduodenoscopy.
3. Endoscopic retrograde cholangiopancreatography (RKhPG).
4. selective angiography.
5. percutaneous cholangiography.
6. Laparoscopy.
7. Laparoscopy with cholecystocholangiography.
8. Computer tomography.
9. radioisotope methods research.
 Application
Table. Differential Diagnostic characteristic some species jaundice
Indicator Suprahepatic H S
s e u
p b
a h
t e
i p
c a
t
i
c
hemolytic shunt hepatic cholestatic stones cancer cancer
hyperbilirubine cellular genera general gall pancreatic
mia l gall duct gland, big
And papilla 12
hepati duodenal
c ducts guts
Age Any, more Any Any Any Mainly mature Mainly Mainly mature
often mature and And elderly
young elderly
pain V areas How rule Missing minor, Minor Intensive colic expressed, expressed,
liver missing Sometimes (in Sometimes indefinite indefinite
sharp period) (in acute character character
intense period)
intense
Fever Appears Absent Possible in Acute stage Often, recurrent recurrent
when acute stages viral, short-term
hemolytic viral, alcoholic, (1-2 days)
crises alcoholic, medicinal
medicinal hepatitis A
hepatitis A
Premonitory How rule How rule For acute At acute Absent Jaundice often Jaundice
period absent absent forms forms precede pain often
diseases diseases precede pain
may be may be
pain, pain,
weakness weakness
Cutaneous How rule How rule Absent Expressed Often, Often, arises Often, arises
itching absent absent intensive periodically periodically

Liver Not Not Always Always Often not More often More often Not
increased increased increased increased enlarged; Not increased increased
or or various various sometimes
increased increased density density increased
slightly slightly and sharp
painful
Spleen More often How rule Not More often Sometime Not increased Not increased How rule Not
increased increased increased s increased increased
Bilirubinuria Absent Absent Available Available Available Arises Arises
Sometimes periodically periodically
absent
Urobilinogen Absent or Absent Available Maybe Often absent Absent Arises
uria insignifica absent periodically
nt
Content Sharp raised Sharp raised IN norm Downgraded IN norm or Absent IN norm,
pigment in or absent absent Sometim
faeces es absent
Content Slightly (in Slightly raised, raised, Much (in Often much Periodicall
bilirubin in 3-5 once) raised, reaction reaction 10 once) (more how in y emerging
blood raised, reaction predominan straight And raised, 20 once) pronounce
reaction indirect tly straight indirect reaction raised, d (bilirubin
indirect predomina reaction rises more
ntly predominantly how in 20
straight straight once)
hyperbiliru
bin-
mission;
reaction
predomina
ntly
straight
Content IN norm IN norm IN norm or Fine or IN norm or IN norm or More often in
cholesterol lowered raised raised raised norm
V blood

Activity IN norm IN norm IN norm or Sharp raised Increased Sharp Sharp

alkaline unsharp increased increased
phosphatase raised

Activity IN norm IN norm Increased More More often More often More often
aminotransfer often increased in norm, in norm,
ases increased Maybe be Maybe be
Sometime increased increased
s in norm
Thymolovaya IN norm IN norm Increased More often IN early stages IN early IN early
try in norm diseases stages stages
(before 1- diseases in diseases in
1.5 months) norm, Later norm,
in norm, increased Later
Later increased
increased